PRACTICAL MEDICINE. 



BY 



F. MORTIMER LAWRENCE, A. M., M. D., 

Assistant in Practice of Medicine, Hahnemann Medical College ; 

Chief of Medical Clinic, Hahnemann Hospital Dispensary, 

Philadelphia. 



PHILADELPHIA : 

BOERICKE & TAFEL. 
1901. 






V 



The library of 

CONGRESS, 

Two Copies Received 

NOV. ?3 1901 

Copyright entry 

CLASS O^ XXo. Mo. 

COPY B. 



Copyrighted 1901, 

BY 
BOERICKE & TAFEL. 



H. B. COCHRAN, PRINTERS, 
LANCASTER, PA. 



TO 

MY MOTHER 



PREFACE. 

This book is intended for students, not advanced workers. 
The endeavor has been to set forth concisely those funda- 
mental facts which are requisite to the successful practice of 
medicine. Pathological processes rather than the details of 
morbid anatomy have been described, with the object of co- 
relating the symptoms of disease to the underlying changes. 
In connection with diagnosis the more important modern 
laboratory methods have been included ; and in addition each 
section is preceded by a brief resume of the essential points 
to be ascertained by interrogation of the patient, and of the 
physical methods by which the examination should be com- 
pleted. 

The work as a whole is based upon the masterly teachings 
of Goodno, and to him in particular must be attributed the 
practical, though necessarily condensed, directions as to treat- 
ment. In the preparation of the articles dealing with semi- 
surgical conditions, notably appendicitis, intestinal obstruction, 
cholelithiasis, and nephrolithiasis, the author has profited 
by the advice and kindly criticism of Dr. William B. Van 
Lennep. The sections devoted to clinical methods and neur- 
ology represent the teachings of Dr. Clarence Bartlett, while 
to Dr. Weston D. Bayley the author is indebted for a careful 
review of that portion of the book dealing with the clinical 
examination of the nervous system. Constant reference has 
been made to the writings of other authorities, however, and 
it is hoped that the work will afford a clear perspective of the 
modern practice of medicine. 

Frederic Mortimer Lawrence. 
October 17, 1901. 



BIBLIOGRAPHY. 

The author acknowledges particular indebtedness to the following works 
and their respective writers: 

Allbutt, T. Clifford: A System of Medicine, 1896. 

Broadbent, William H.: Heart Disease, 1900. 

Bury, Judson S. : Clinical Medicine, 1894. 

Butler, G. R. : Diagnostics of Internal Medicine, 1901. 

Cabot, Richard C. : Examination of the Blood, 1901. 

Cabot, Richard C : Physical Diagnosis, 1900. 

Church, A. and Peterson, F. : Nervous and Mental Diseases, 1900. 

Coles, A. C: Diseases of the Blood, 1898. 

Finlayson, James: Clinical Manual, 1891. 

Fowler, J. K., and Godlee, R. J. : Diseases of the Lungs and Pleurae, 1898. 

Goodno, William Q.: Practice of Medicine, 1896. 

Herter, Christian: Diagnosis of Diseases of the Nervous System, 1892. 

Hutchison and Rainy: Clinical Methods, 1897. 

Hughes, Richard: Manual of Pharmacodynamics, 1886. 

Klemperer, G. : Clinical Diagnosis, 1898. 

Musser, John H.; Medical Diagnosis, 1900. 

Osier, William: Practice of Medicine, 1901. 

Purdy, Charles: Practical Urinalysis and Urinary Diseases, 1900. 

Raue, C. G. : Special Pathology and Therapeutics, 1895. 

Raue, C. S.: Diseases of Children, 1899. 

Reference Handbook of the Medical Sciences, 1901. 

Striimpell, A.: Practice of Medicine, 1901. 

Thompson, H. Campbell: Nervous Diseases, 1899. 

Twentieth Century Practice of Medicine, 1900. 

Tyson, James: Practice of Medicine, 1901. 



CONTENTS. 



PRACTICAL MEDICINE. 



INFECTIOUS DISEASES. 



General Considerations, 17 

Periods of Incubation and Infectiousness, 19 

The Clinical Aspects of Infectious Disease, " . . . 20 

The Diagnosis of Infectious Diseases, 21 

The Treatment of Infectious Diseases, 23 

Typhoid Fever, 25 

Typhus Fever, 32 

Relapsing Fever, 35 

Dengue, 37 

Miliary Fever, 39 

Influenza, 40 

Yellow Fever, 41 

Dysentery. 43 

The Malarial Fevers, 45 

Rheumatic Fever, 51 

Cerebro-Spinal Fever, 53 

Pneumonic Fever, 55 

Asiatic Cholera, . . 59 

Diphtheria, 61 

Erysipelas, 63 

The Septic Fevers, 65 

Sapremia, ... 65 

Septicemia, 66 

Pyemia, 67 

Scarlet Fever, 68 

Measles, 71 

Rubella, 73 

Variola, 74 

Vaccination, , 76 

Varicella, .77 

Whooping Cough, ■ ■ 78 

Mumps, • 79 



8 CONTENTS. 

PAGE. 

Tetanus, 80 

Anthrax, 82 

Rabies, 83 

Glanders, 84 

Actinomycosis, 86 

Tuberculosis, 87 

Acute Tuberculosis, 89 

Typhoid Form, . . 89 

Pulmonary Form, 90 

Meningeal Form, . 91 

Tuberculosis of the Lymphatic Glands, 92 

Pulmonary Tuberculosis, 93 

Caseous Tuberculosis of the Lungs, 95 

Fibroid Tuberculosis of the Lungs, > 96 

Chronic Pulmonary Tuberculosis, > 97 

Syphilis, 104 

Acquired Syphilis, 105 

Hereditary Syphilis, 107 

Leprosy, 109 

The Plague, in 

DISEASES OF THE CIRCULATORY SYSTEM. 

General Considerations, .... 113 

Physical Examination of the Heart and Arteries, 114 

Inspection and Palpation, 114 

Percussion, 115 

Auscultation, 116 

The Pulse, 119 

Diseases of the Pericardium, 121 

Pericarditis, 121 

Hydropericardium, 123 

Hemopericardium, 123 

Pneumopericardium, 128 

Diseases of the Endocardium, 123 

Endocarditis, , . 123 

Chronic Vavlular Diseases of the Heart, 125 

Mitralinsufficiency, • . . . 125 

Mitral Stenosis, ; 126 

Aortic Insufficiency, 127 

Aortic Stenosis 128 

Tricuspid Insufficiency, 129 

Tricuspid Stenosis, .129 

Pulmonic Valve Lesions, 129 



CONTENTS. 9 

PAGE. 

Diseases of the Myocardium, 131 

Hypertrophy of the Heart, 131 

Dilatation of the Heart, 133 

Acute Myocarditis, 134 

Chronic Myocarditis, 135 

Degenerations of the Heart Muscle, 135 

Neuroses of the Heart, 136 

Palpitation, .... 136 

Tachycardia, 137 

Bradycardia, 137 

Arhythmia, 137 

Angina Pectoris, 138 

Diseases of the Blood Vessels, 140 

Arterio-Sclerosis, 140 

Aneurism, 142 

Aneurism of the Thoracic Aorta, 142 

DISEASES OF THE RESPIRATORY SYSTEM. 

General Considerations, 147 

Diseases of the Upper Respiratory Tract, 147 

Clinical Examination of the Upper Air Passages, 148 

Acute Rhinitis, 150 

Chronic Rhinitis, .... . . 151 

Hay Fever, . 152 

Acute Catarrhal Laryngitis, 153 

Chronic Catarrhal Laryngitis, 154 

Edematous Laryngitis, .... 154 

Tubercular Laryngitis, 155 

Syphilitic Laryngitis, 155 

Diseases of the Lower Respiratory Tract, 156 

Physical Examination of the Respiratory Organs, 157 

Inspection, 157 

Palpation, 160 

Percussion, . . . . 161 

Auscultation, 162 

Bronchitis, 164 

Acute Simple Bronchitis, 165 

Capillar}- Bronchitis, 166 

Chronic Bronchitis, . . 168 

Plastic Bronchitis, 169 

Bronchiectasis, 169 

Asthma „ 171 



10 CONTENTS. 

PAGE. 

Congestion of the Lungs, 172 

Active, . . . . 172 

Passive, 175 

Edema of the Lungs, , 173 

Hemoptysis 174 

Emphysema, 175 

Interlobular or Interstitial Emphysema, ". . 175 

Vesicular Emphysema, 175 

Broncho-Pneumonia, 177 

Gangrene of the Lungs, 179 

Abscess of the Lung, . 180 

Tumors of the Lung, 181 

Collapse of the Lung, 181 

Pleurisy, . . . 183 

Dry Pleurisy, 183 

Pleurisy with Effusion, 183 

Empyema, 183 

Pneumothorax, 187 

Hydrothorax, 189 

Hemothorax, 189 

DISEASES OF THE URINARY SYSTEM. 

General Considerations, 191 

Examination of the Urine, 193 

Physical Examination of the Urine, 194 

Chemical Examination of the Urine, 196 

Normal Constituents, 196 

Pathological Constituents, 198 

Microscopical Examination of the Urine, 201 

Chemical Sediments, 202 

Anatomical Sediments, 205 

Uremia, 208 

Acute Hyperemia of the Kidney, 209 

Chronic Hyperemia of the Kidney, 210 

The Classification of Bright's Disease, 210 

Acute Parenchymatous Nephritis, 211 

Chronic Parenchymatous Nephritis, 213 

Chronic Interstitial Nephritis, 215 

Amyloid Kidney, 218 

Pyelonephritis, 218 

Tuberculosis of the Kidney, 219 

Nephrolithiasis, 222 

Hydronephrosis, . 224 

Floating or Movable Kidney, 226 



CONTENTS. 11 

PAGE. 

Cystitis, . . 227 

Incontinence of Urine 228 

DISEASES OF THE DIGESTIVE TRACT. 

Affections of the Mouth and Throat, 231 

Stomatitis, 232 

Glossitis, 233 

Acute Tonsillitis, 234 

Hypertrophy of the Tonsils, 235 

Acute Catarrhal Pharyngitis, .... 236 

Chronic Pharyngitis, . . . . 237 

Retropharyngeal Abscess, 238 

Acute Esophagitis, 238 

Stenosis of the Esophagus, 238 

Diseases of the Stomach and Intestines, 239 

External Examination, 241 

Examination of the Stomach Functions, 242 

Examination of the Feces, 246 

Acute Gastritis, . 249 

Chronic Catarrhal Gastritis, 250 

Ulcer of the Stomach, . 253 

Cancer of the Stomach, 256 

Dilatation of the Stomach, 258 

Hematemesis, 259 

Gastric Neuroses, 260 

Nervous Dyspepsia, 261 

Hyperchlorhydria, 262 

Gastralgia, 263 

Splanchnoptosis, 263 

Acute Enteritis, 265 

Chronic Enteritis, 267 

Cholera Morbus, 268 

The Diarrheas of Children, .268 

Intestinal Obstruction, 271 

Acute Obstruction, . . . . 271 

Chronic Obstruction, 272 

Appendicitis, 274 

Constipation, 279 

Intestinal Cancer, 280 

Intestinal Neuroses, 281 

Diseases of the Peritoneum, 282 

Acute Peritonitis, 282 

Chronic Peritonitis, 184 

Ascites, 285 



12 CONTENTS. 

PAGE. 

Diseases of the Liver and Gall Ducts, 286 

Physical Examination of the Liver, 278 

Malformations and Malpositions of the Liver, 290 

Circulatory Affections of the Liver, 291 

Passive Hyperemia of the Liver, ; 291 

Perihepatitis, 292 

Abscess of the Liver, . . . 293 

Cirrhosis of the Liver, 295 

Amyloid Degeneration of the Liver, 299 

Acute Yellow Atrophy of the Liver, 300 

Fatty Liver, 302 

Cancer of the Liver, 302 

Jaundice, 304 

Icterus Neonatorum, 306 

Simple Catarrhal Jaundice, 307 

Cholelithiasis, 308 

Diseases of the Portal Vein, 313 

Diseases of the Pancreas, 314 

Diseases of the Spleen, . . . . 317 

DISEASES OF THE BLOOD. 

General Considerations, 321 

Clinical Examination of the Blood, 321 

Symptomatic Anemia, 330 

Chlorosis, 332 

Pernicious Anemia, 333 

Leucocythemia, 334 

Splenic Anemia, . . 336 

Hodgkin's Disease, 337 

Anemia Infantum Pseudo-Leukemia, 338 

Hemophilia, 339 

Purpura, • . . 340 

Scurvy, 34 1 

Infantile Scurvy, 34 2 

DISEASES OE THE DUCTEESS GEANDS. 

Addison's Disease, 343 

Goitre, 344 

Exophthalmic Goitre, 345 

Myxedema, 347 

CONSTITUTIONAL DISEASES. 

Diabetes Mellitus, 349 

Diabetes Insipidus, 35 2 



CONTENTS. . 13 

PAGE. 

Gout 353 

Arthritis Deformans, 356 

Rickets, . . 358 

Osteomalacia, 359 

Obesity, , . . . 359 

DISEASES OE THE NERVOUS SYSTEM. 

General Considerations, 361 

Examination of the Nervous System, 362 

The Intellectual Functions, 363 

Cranial Nerve Functions, 365 

Motor Functions 374 

Sensory Functions, . . . . ...... 385 

Reflex Functions, 387 

Cerebral Localization, 390 

Diseases of the Brain and its Membranes, 391 

Pachymeningitis, 391 

Leptomeningitis, 392 

Hydrocephalus, .... 394 

Cerebral Anemia, . 396 

Cerebral Hyperemia, 397 

Intracranial Hemorrhage, 398 

Cerebral Softening, 402 

Intracranial Tumor, 404 

Acute Hemorrhagic Encephalitis, 407 

Purulent Encephalitis, 407 

Superior Acute Encephalitis, 408 

Superior Chronic Polioencephalitis, 409 

Inferior Polioencephalitis, 410 

Infantile Cerebral Palsies, 411 

Paralytic Dementia, 412 

Disseminated Cerebro-Spinal Sclerosis, 414 

Diseases of the Spinal Cord and its Membranes, 416 

Spinal Leptomeningitis, 417 

Spinal Hemorrhage, 418 

Acute Ascending Paralysis, 419 

Myelitis, 420 

Acute Anterior Poliomyelitis, 423 

Chronic Anterior Poliomyelitis, .... 424 

Amyotrophic Lateral Sclerosis, 425 

Spastic Paraplegia, 426 

Ataxic Paraplegia, 427 

Hereditary Ataxia, , 429 



14. CONTENTS. 

PAGE. 

Locomotor Ataxia, 430 

Syringomyelia, 433 

Caisson Disease, 435 

Diseases of the Peripheral Nerves, 435 

Neuritis, 435 

Neuralgia, 439 

Syphilis of the Nervous System, 440 

The Neuroses, 442 

Hysteria, 442 

Epilepsy, 449 

Neurasthenia, 453 

Chorea, 456 

Tetany, 458 

Choreiform Diseases, 459 

Huntingdon's Chorea, 459 

Habit Chorea, 460 

Electrical Chorea, 460 

Myoclonus, 460 

Paralysis Agitans, 460 

Occupation Neuroses, 462 

Migraine, 462 

Traumatic Neuroses, 464 

Tics, 465 

Trophoneuroses, 466 

Acromegaly, . 466 

Raynaud's Disease, 467 

Angioneurotic Edema, 468 

Scleroderma, 468 

Facial Hemiatrophy, 469 

Infantile Convulsions, 469 

Disorders of Sleep, 471 

Insomnia, 471 

Sumnambulism, .••... 471 

Narcolepsy, 472 

Catalepsy, . 472 

Sunstroke, 472 

Heat Exhaustion, 472 

Thermic Fever, 473 



CONTENTS. 15 



PAGE. 

DISEASES OF THE MUSCLES. 

Myositis, 477 

Primary Myositis, 477 

Acute Simple Myositis, 477 

Acute Infectious Myositis, 477 

Acute Infectious Poliomyositis, 477 

Chronic Progressive Ossifying Myositis, 478 

Secondary Myositis, 478 

Rheumatic Myositis, 479 

Myotonia Congenita, 479 

Progressive Muscular Dystrophy, 480 

THE INTOXICATIONS. 

Alcoholism, 483 

Morphinism, 485 

Chloralism, 485 

Cocainism, ... 486 

Plumbism, 486 

Arsenical Poisoning, 487 

Ptomaine-Poisoning, 4S8 

ANIMAL PARASITIC DISEASES. 

Cestodes, 491 

Taenia Solium, 491 

Taenia Saginata, 492 

Bothriocephalus Hiatus, 492 

Taenia Echinococcus, 492 

Trematodes, 493 

Liver Flukes, 493 

Blood Flukes, 494 

Bronchial Flukes, .... 494 

Nematodes, 494 

Ascaris Tumbricoides, 494 

Oxyuris Vermicularis, 494 

Trichina Spiralis, 495 

Anchylostoma Duodenale, 496 

Tricocephalus Dispar, 496 

Filaria Sanguinis Hominis, 496 

Index, 498 



INFECTIOUS DISEASES. 



An infectious disease is one caused by the invasion and repro- 
duction within the body of pathogenic micro-organisms. 

Contagion, the direct communication of disease from one 
person to another, occurs in those infectious diseases in which 
the virus is discharged from the body by channels which 
render its transportation to another easy. For example, in 
scarlatina, measles and smallpox the virus is eliminated by 
the skin, tiny scales of which are easily carried by the air. 
On the other hand, in malaria the virus is not discharged at 
all, and contagion is unknown; while in typhoid it is elimin- 
ated only in the urine and feces, and ordinary cleanliness 
renders contagion impossible. 

Infection is conveyed by various media, including: 

1. Fomites, i. e., substances, such as clothing, furniture and 
domestic animals, which have been in direct contact with the 
infected patient. Smallpox and diphtheria in particular are 
apt to be conveyed in this manner. 

2. Water. — This may become contaminated with the dis- 
charges of infected patients. Typhoid and cholera are among 
the diseases thus conveyed. 

3. Milk. — This may convey contagion from a tuberculous 
cow, but more often it is contaminated by water used to wash 
the milk cans. Typhoid epidemics have originated in this 
way. 

2 



18 INFECTIOUS DISEASES. 

4. Dust. — Particles of dust frequently carry with them micro- 
organisms. In particular, the sputum of tuberculous patients, 
drying in the air, is caught up with the dust and the bacteria 
enter the lungs with the inspired air. 

5. Insects, etc. — Typhoid, cholera, etc., may be spread by 
flies, which after contact with the infected excreta, carry the 
virus to deposit it on food; malaria is conveyed by mosquitoes, 
and bubonic plague by rats. 

6. Atmospheric air was formerly regarded as a carrier of 
infection, but it is probable that the responsibility rests with 
dust, insects, etc., rather than with the air itself. 

Infective agents gain access to the body through the respira- 
tory system, through the intestinal system, or through some 
break in the skin. At the point of invasion the micro-organ- 
isms are met by resistance on the part of the organism (phago- 
cytosis?) and are either destroyed or, having gained a foothold, 
proceed to a rapid reproduction; while coincidently with their 
rapid increase in numbers they elaborate certain chemical 
products which, disseminated through the body, act as violent 
toxins. In case the body can overcome the invaders at the 
outset, the individual is said to be immune ; if, however, the 
infective agents are successful in overcoming the resistance of 
the body, the individual is said to be susceptible. 

Immunity, the resistance of the living organism to infection, 
varies greatly in different individuals. It occurs in two forms: 
natural immunity, the natural and constant resistance of a 
healthy animal to certain diseases; and acquired immunity, 
the resistance resulting from accidental circumstances such as 
a previous attack of the same disease (yellow fever, etc.). In 
addition an experimental immunity may be induced by various 
laboratory manipulations. 

As a corollary to these facts, it follows that susceptibility to 
infection varies widely in different animals, in different races, 
in different men, and in the same man at different times. In 
man this susceptibility is influenced by — 

1. Race. — For example, the negro races resist infection with 



INFECTIOUS DISEASES. 19 

malaria or yellow fever, but are particularly susceptible to 
smallpox and tuberculosis. 

2. Heredity. — A family predisposition to certain fevers is 
•common. Cancer and tuberculosis are regarded as diseases 
more or less hereditary. It is necessary, however, to consider 
the possible greater exposure to infection in these cases as, 
for instance, in the case of a child with a tuberculous parent. 

3. Environment. — -The influence of certain seasons, exposure 
to extremes of temperature, fatigue, and starvation tend to 
abolish resistance to micro-organic invasion in individuals not 
ordinarily susceptible. 

4. Pre-existing Diseases. — Certain pre-existing lesions afford 
ready ingress and suitable environment for pathogenic micro- 
organisms. For instance, diabetic patients are particularly 
susceptible to the tubercle bacillus. 

5. Dosage of Bacteria. The severity of an infection is, to 
a certain degree, in direct proportion to the amount of the 
virus. 

The aim of modern investigators is to discover the means 
"by which nature induces immunity in the individual, and to 
apply this knowledge toward the prevention and cure of dis- 
ease. Their results thus far are embodied in the various 
therapeutic serums. 

PERIODS OF INCUBATION AND INFECTIOUSNESS. 

The time elapsing between the invasion of the organism 
and the development of the symptoms is known as the period 
of incubation. It varies considerably in the same disease ac- 
cording to the virulence of the infection and the susceptibility 
of the patient. The period of infectiousness represents the 
time during which the individual is liable to communicate the 
disease to others, and during which, in consequence, isolation 
and other precautions should be continued. 



20 



INFECTIOUS DISEASES. 



INCUBATION. 


Typhoid, 


7-22 days. 


Typhus, 


5-21 days. 


Relapsing, 


5-16 days. 


Dengue, 


3-5 days. 


Influenza, 


1-5 days. 


Yellow Fever, 


1-14 days. 


Malaria, 


6-21 days. 


Asiatic Cholera, 


1-7 days. 


Diphtheria, 


2-7 days. 


Scarlatina, 


2-10 days. 


Measles, 


7-14 days. 


Rubella, 


5-21 days 



Small-pox, 8-15 days. 

Chicken-pox, 12-19 days. 

Whooping Cough, 7-14 days. 
Mumps, 14-25 days. 

Bubonic Plague, 3-6 days. 



INFECTIOUSNESS. 

Onset to end of second week of convalescence. 

Onset to end of three weeks. 

Onset to end of one week. 

Onset to end of one week. 

Onset to end of two weeks. 

Onset to end of one week. 

Onset to disappearance of plasmodium. 

Onset to end of one week. 

Incubation to three weeks or more after con- 
valescence. 

Onset to end of desquamation. 

Earliest prodromes to three weeks after 

recovery. 
Three days before rash to end of desquama- 
tion. 

Onset to end of desquamation. 

Onset to end of desquamation. 

Onset to end of whooping period. 

Onset to end of three weeks. 

Onset to disappearance of symptoms. 



In many of these diseases, particularly smallpox and diph- 
theria, conveyance of infection by fomites is possible for 
periods of months and even years. Only by thorough disin- 
fection can this be prevented. 

THE CLINICAL ASPECTS OF INFECTIOUS DISEASE. 

The clinical manifestations attending infectious disease are, in gen- 
eral, those indicated' by the term fever. They include eleva- 
tion of temperature {pyrexia), acceleration of pulse and 
respiration, disturbances of the gastrointestinal and nervous 
systems (nausea, vomiting; pain, delirium), and scanty, con- 
centrated urine. 

Various types of fever are recognized, including: 

1. Continued fever. — In which the daily variation in tem- 
perature is slight (1-2°). 

2. Remittent fever. — In which the daily temperature varia- 
tion is marked but the minimum is still above normal. 

3. Intermittent fever. — In which the temperature variation 
is marked and falls to or below normal. 



INFECTIOUS DISEASES. 21 

4. Inflammatory fever. — Symptomatic of some localized in- 
flammation. 

The course of fever is divided into: 

1. The onset, or period of invasion, during which the 
temperature continues to rise. 

2. The " fasti gium" or period during which the temper- 
ature remains at its acme. 

3. The period of decline or " defervescence." In this stage 
death may be ushered in by either hyperpyrexia (above 
105.5°) or collapse (below 96°); or the fever may terminate 
abruptly (crisis) or gradually (lysis) and convalescence be 
established. 

The typhoid, i. e., typJins-like state is a condition present 
in many fevers. It is characterized by a dry brown tongue 
and sordes upon teeth and gums; feeble heart with weak, 
rapid pulse; faulty circulation, resulting in superficial inflam- 
matory and destructive changes (bed sores), and muttering 
delirium, stupor, twitchings, tremor and sinking to the foot of 
the bed. 

The diagnosis of infectious diseases depends upon the careful in- 
terrogation and physical examination of the patient. 

A. The interrogation should embrace: 

1. A Jiistory of previous infections diseases. Yellow fever, 
scarlatina and measles usually confer immunity to a second 
attack, while rheumatism and pneumonia predispose to a re- 
currence. 

2. Possible cause of the present attack (exposure to infec- 
tion; general influence of patient's environment; and also any 
localized inflammation which may in itself have given rise to 
the pyrexia). 

3. The mode of onset (prodromal symptoms, as in typhoid, 
or sudden invasion, as in scarlatina, cholera, etc.,) often 
affords a diagnostic clew. 

B. The physical examination should include: 

1. The temperature. This should be ascertained by insert- 



22 INFECTIOUS DISEASES. 

ing a clinical thermometer into the mouth, axilla or rectum for a 
period of five minutes or more. The normal temperature in 
the mouth is 98.4° F. ; that in the axilla is slightly lower, 
while in the rectum it is somewhat higher. 

In investigating an infectious disease the temperature should 
be taken not once, but twice daily, at stated hours in the morn- 
ing and evening. The variation determines the type of fever 
and assists both diagnosis and prognosis. 

2. Characteristic signs. Inspection will reveal the various 
skin eruptions, etc., as well as aid in determining the condi- 
tion of the sensorium (for example, the apathy of typhoid, 
meningitis and severe sepsis). 

3. The physical condition of heart, lungs, kidneys and 
digestive tract. An exact knowledge of the state of these 
organs is of the utmost importance, for upon their integrity 
and their ability to bear the brunt of the attack recovery 
depends. Until this is ascertained a prognosis cannot be 
framed or a proper course of treatment directed. 

The Management of an Infected Patient demands immediate at- 
tention from the physician. This implies: 

1, Isolation of the patient. Let him be put to bed in a large 
upper room with good light and ventilation, all upholstery, 
curtains and unnecessary furniture being removed before the 
entrance of the patient. Allow no one else but the attendants 
to enter, and have each one take every precaution against 
conveying contagion from the room. The door should be 
screened with a sheet kept moist with some disinfecting fluid. 

2. Cleanliness. The entire body of the patient should be 
cleansed with warm water and soap at least once daily. The 
mouth and teeth should be scrubbed frequently with a 
solution of boric acid or some other mild antiseptic. The bed 
clothing should be changed daily and must be disinfected be- 
fore it leaves the room. All discharges should be received 
and allowed to remain for a time in vessels containing a germi- 
cidal solution. At the conclusion of the illness the patient 
and attendants should bathe, apply a disinfecting solution to 



INFECTIOUS DISEASES. 23 

the body, don fresh clothing and leave the room immediately. 

3. Disinfection of the Room. As soon as the room is va- 
cated every inch of it should be cleaned with soap, water and 
disinfecting solutions. The paper should be removed from 
the walls and the woodwork repainted at once. 

The Treatment of an Infected Patient consists, in great measure, 
of rest, careful nursing, a proper diet, and the treatment of 
individual symptoms as they arise. 

Diet. — Patients must be individualized, but a majority of 
them thrive best on a strictly liquid diet. Good milk, admin- 
istered in definite quantities at stated intervals (in adults, 
from two to four ounces every two hours) is best. Animal 
broths, eggs, and long-cooked gruels are occasionally desir- 
able. Pure water should be given freely; and in cases pre- 
senting profound toxemia the latter may be supplemented by 
the introduction subcutaneously of large quantities of the 
normal saline solution. 

Hydrotherapy. — At least one daily bath, with soap and 
warm water, is essential to cleanliness. In many of the in- 
fectious diseases the external use of water affords a simple 
and harmless means of reducing the temperature and con- 
trolling the extreme pyrexia. Among the more important 
methods for accomplishing this are the following: 

The Sponge Bath. — The bed is protected by mackintosh or 
rubber sheeting, and a sponge or wash-cloth is saturated with 
water, the latter being at room-temperature or cooled with 
ice. Every portion of the patient's body is in turn bared, 
washed with moderate friction, and dried. In case the tem- 
perature is high it is well to dry the skin by fanning it rather 
than with cloths, thus aiding the abstraction of heat by 
evaporation. The sponging may be repeated every one, two, 
or three hours, according to the height of the temperature; it 
adds greatly to the comfort of the patient, but reduces the 
pyrexia so slightly, unless the water be very cold and applied 
frequently, that in severe cases it is wiser to resort to other 
methods. 



24 INFECTIOUS DISEASES. 

Cold Compi'esses. — Three or four thicknesses of old table 
linen or toweling are moistened with cool water and applied 
to the body; and a second compress is applied as soon as the 
first one becomes warm. While agreeable to the patient, the 
compress has little effect upon temperature. 

The " cheese-cloth bath" highly recommended by Goodno, 
consists of about four layers of cheese cloth dipped in ice 
water and then wrung out almost dry. The patient lies upon 
his side, a single layer of dry cheese cloth is placed over his 
body, and the moistened layers are laid over him so as to 
cover the body anteriorly, laterally, and posteriorly, from 
neck to knees. By this agreeable method heat is dissipated 
rapidly and the temperature quickly falls. 

Tlie Cold Pack. — A blanket is laid smoothly over the bed, 
and on it are spread one or more sheets wrung out in cold 
water. The patient is placed in the middle of the sheets and 
the latter quickly wrapped about him, and then the blanket 
is folded over all. At the end of half an hour the patient 
begins to feel warm and often perspires freely, though the 
temperature is considerably reduced. When it begins to rise 
again the pack may be repeated. 

The cold bath, advocated by Brand and others and ex- 
tensively used in Germany, must be instituted during the first 
week of the disease if at all. When the patient's temperature 
reaches 102.2° F. he is placed for about fifteen minutes in a 
bath tub containing water at 65-70°, and during this time he 
is rubbed by attendants. On entering the bath he receives 
about an ounce of whisky, well diluted, or half a glassful of 
wine. At the conclusion of the bath he is lifted to his bed, 
which is spread with a rubber sheet, and covered with a 
blanket. In ten or fifteen minutes he is thoroughly dried and 
his night dress replaced, and he is then given a cup of milk or 
broth. As long as the temperature remains high the bath is 
repeated every three hours. This method, while of undoubted 
efficacy, is little used in private practice. 

Stimulants should be administered to an infected patient 



INFECTIOUS DISEASES. 25 

only upon the presence of well-defined indications for their 
use, such as are afforded by progressive enfeeblement of the 
heart, high delirium, pulmonary consolidation, or great ab- 
dominal distention. 

Convalescence demands great care in the resumption of 
ordinary habits of exercise, diet, etc. Solid food should be 
added to the dietary by degrees, and mental and physical ex- 
ercise should be forbidden until the wasted body has had an 
opportunity to recuperate. 

TYPHOID FEVER. 

(Abdominal typhus; enteric fever.) 

Etiology. — The exciting cause is the bacillus typhosus of 
Eberth. It is transmitted principally in drinking water con- 
taiminated with the discharges from typhoid patients. 

Autumn, early adult life and individual susceptibility con- 
stitute predisposing factors. 

Pathology. — The essential lesions are: 

1. Changes in the intestinal lymphoid glands. During the 
first week the solitary follicles and Peyer's glands become 
swollen and congested, with, perhaps, beginning ulceration. 

During the second week ulceration continues and some 
sloughing takes place. 

During the third week sloughing continues, leading some- 
times to coalescence of adjacent lesions, or to perforation. 

During the fourth week some ulceration and sloughing con- 
tinue, but cicatrization begins, and ultimately there are left 
smooth depressed scars. 

2. Changes in the mesenteric glands are similar to those in 
the intestine, but as the products of necrosis cannot be thrown 
off they form purulent foci which become encapsulated or ab- 
sorbed on recovery. They may rupture into the peritoneal 
cavity. 

3. The spleen becomes enlarged and hard. 



26 INFECTIOUS DISEASES. 

4. The toxemia causes various complicating lesions, includ- 
ing the following: 

{a.) The liver, is enlarged and softened, and its cells may 
undergo granular and fatty degeneration. 

(&.) The kidneys show parenchymatous degeneration, and 
occasionally acute nephritis or infarction occurs. 

(r. ) The heart muscle is degenerated, becoming soft and 
flabby. 

(d. ) The respiratory tract is the seat of catarrhal changes, 
while hypostatic congestion of the lungs is the rule and catar- 
rhal pneumonia is common. 

(e. ) The nervous system and the glandular structures un- 
dergo inflammatory changes occasionally. 

(/".) The general mus cnlar system is degenerated. 

Clinical Course. — After a prodromal period of a week or ten 
days during which the patient surfers with lassitude, headache, 
slight digestive disturbances, and often epistaxis, the initial 
stage is ushered in by a gradual, step-like rise of temperature 
day by day for a week. During this first week there is pros- 
tration, severe headache, and gastro-intestinal disorder. 

The second week is marked by continued fever and aggrava- 
tion of the existing symptoms. The tongue becomes dry and 
fissured; rose spots appear on the abdomen; the enlarged 
spleen is recognizable by palpation; and the headache gives 
way to mental apathy or mild delirium. The pulse becomes 
frequent; diffuse bronchitis is usually present; the abdomen is 
distended; there may be constipation or diarrhea; and pros- 
tration grows more and more profound. 

The third Week shows a temperature that is still high, but 
in favorable cases the morning remissions become more 
marked. The pulse js rapid and feeble, the heart's impulse 
weak; muttering delirium alternates with apathy; emaciation 
and prostration are extreme. There may be retention of 
urine or incontinence of feces. At this period there is danger 
of hemorrhage, perforation, and peritonitis, and pulmonary 
complications. 



INFECTIOUS DISEASES. 



27 



In the fourth week the temperature becomes normal and the 
symptoms subside. 

Analysis of Symptoms. — Fever. — In typical cases the tempera- 
ture rises gradually, being higher in the evening than in the 
morning, until at the end of a week it has reached 103° or 
104°. During the second week it remains fairly stationary at 
the maximum, with slight morning remissions. In the third 
week the morning remissions become more marked, the even- 
ing maximum remaining unchanged. In the fourth week the 




Fig. I. The Typical Temperature Curve of Typhoid Fever. (Salinger- 

Kalteyer.) 

fever terminates by lysis, the morning temperature reaching 
normal or subnormal, and the evening rise growing less each 
day until it too is normal. 

Variations from this typical course are common. In some 
cases the temperature rises quite abruptly at the onset, reach- 
ing its maximum on the second or third day. In some mild 
cases it may never rise above 101°, although if the other 
symptoms are severe this low temperature is not a favorable 



28 INFECTIOUS DISEASES. 

sign. A rapid rise late in the course of the disease indicates 
the onset of a serious complication. A sudden fall suggests 
hemorrhage or perforation. 

Circulatory Symptoms. — With the rise of the temperature 
the pulse becomes full and dicrotic, and at the end of the first 
week its frequency is about 100. During the second and third 
weeks it becomes quicker and feeble in direct proportion to 
the gravity of the case. The heart becomes weak, the first 
sound losing intensity until it resembles the second. The 
cardiac weakness permits a circulatory stasis which may result 
in hypostatic pneumonia, venous thrombosis, embolism, etc. 

Nervous Symptoms. —During the first week headache is 
pronounced, and often is associated with sleeplessness and rest- 
lessness at night. In the second week these symptoms give 
way to mental apathy or delirium, the latter varying from a 
simple confusion of ideas to an acute mania. Later, delirium 
becomes profound, and with it there may be tremor, twitch- 
ing (subsultus tendinum), and picking at the bed clothes or 
imaginary objects. 

Respiratory Symptoms. — Bronchitis in some degree con- 
stantly accompanies typhoid; there may be rapid respiration, 
slight cough and bronchial rales. Lobular pneumonia is a less 
frequent complication, while lobar pneumonia is rare. 

Abdominal Symptoms.- — Pain and tenderness, especially in 
the right iliac fossa in association with gurgling on pressure, 
are symptoms generally present but by no means pathogno- 
monic. Tympanites, due to paresis of the bowel, develops 
in the second week in most cases. Diarrhea, with stools like 
pea-soup, is often present, although at times constipation is 
persistent. 

Hemorrhages from the bowels are of serious import; for the 
loss of blood, resulting from the erosion of vessels by the 
intestinal lesion, may be sufficient to destroy life at once. 
Hemorrhage is always a grave symptom, denoting extensive 
ulceration. 

The eruption of typhoid is characteristic. It appears on 



INFECTIOUS DISEASES. 29 

the abdomen or other parts of the trunk at the close of the 
first week, and consists of several small rose-colored macules, 
resembling flea bites, which disappear on pressure. Several 
crops appear on successive days. In some cases, particularly 
in children, the eruption is absent. 

The urine presents the changes peculiar to the febrile 
state. At first it is reduced in quantity and of high color and 
specific gravity. Later in the disease, it is apt to contain a 
little albumen and a few casts, the latter indicating paren- 
chymatous degeneration of the kidney. 

Complications. — Any aggravated symptom, such as high tem- 
perature or excesive diarrhea, may be regarded as a compli- 
cation. Among other complicating features, all of which occur 
most frequently in the third week, are intestinal hemorrhage, 
peritonitis, glandular abscesses, otitis media, venous throm- 
bosis, nephritis, and pneumonia (catarrhal, rarely croupous). 

Varieties. — Walking Cases. — These are mild cases in which 
the symptoms are so slight that the patient keeps about for a 
week or two. Nevertheless the intestinal lesions may progress 
rapidly, and grave symptoms, the result of perforation, may 
develop suddenly. 

Abortive Cases. — This term is applied to cases which run a 
typical typhoid course for a week or two, and then all 
symptoms subside and convalescence ensues. 

A Relapse is a second typical attack of typhoid immediately 
following a first and is supposed to be due to re-infection. 

A Recrudescence is a sudden but temporary elevation of tem- 
perature, without aggravation of symptons, occurring during 
convalescence. 

Diagnosis. — The majority of cases of continued fever met in 
this region, not due to pulmonary tuberculosis, are typhoid in 
character. It is well, therefore, to regard all doubtful cases 
as probably typhoid, reserving a positive diagnosis until the 
development of characteristic symptoms, such as the peculiar 
temperature curve, the enlarged spleen, and the eruption, es- 
tablishes the identity of the disease. 



30 INFECTIOUS DISEASES. 

Elirlicli s diazo-re action, which appears in the urine about 
the close of the first week, may aid in diagnosis occasionally. 
Two solutions are required: (1) a 0.5% solution of sodium 
nitrite; (2) a mixture of 2 grams of sulfanilic acid, 150 c.c. hy- 
drochloric acid, and 1000 c.c. of distilled water. One part of 
the first solution is mixed with forty parts of the second, an 
equal quantity of urine and about one-eighth volume of 
ammonium hydrate are added, and the whole is shaken well. 
To constitute a positive reaction both foam and fluid should 
"become bright red in color. This reaction may be present in 
acute tuberculosis, meningitis, measles and other febrile affec- 
tions; hence its diagnostic value is limited. 

The Widal serum test yields a positive reaction in almost 
all cases of typhoid after the eighth day and often earlier. A 
drop of blood from a needle-prick of the ear or finger of the 
patient is allowed to dry upon a clean glass slide. A loopful of 
a fresh bouillon-culture of tvphoid bacilli is placed upon a clean 
cover glass and to this is added a large loopful of a watery so- 
lution of the dried blood. The cover glass is inverted over the 
concavity of a hollow slide and sealed at the edges. Under a 
high power lens a rapid clumping of the bacilli can be ob- 
served in the hanging drop and their movement ceases almost 
instantly. If this reaction cannot be obtained at the end of a 
week typhoid can be excluded; but its appearance, on the 
other hand, may be the result of an attack ten years previ- 
ously. 

Acute miliary tuberculosis resembles typhoid very closely. 
The high remittent fever, the preponderance of pulmonary 
over abdominal symptoms, the consolidation at the apices 
rather than the base of the lungs, and the absence of erup- 
tion may serve to distinguish it. 

Gastro-enteritis in children, with marked abdominal symp- 
toms, may simulate typhoid. Greater fever, profound pros- 
tration, an enlarged spleen and the characteristic eruption 
indicate the latter, however. 

Prognosis. — While generally favorable, the death-rate under 



INFECTIOUS DISEASES. 31 

skillful treatment being less than ten per cent., the prognosis 
is influenced by three considerations, viz., 

1. The severity of the infection. Hyperp} T rexia or profound 
toxemia and the resulting severe nervous symptoms are of un- 
favorable significance. 

2. Personal factors. A history of family susceptibility, pre- 
existing lesions of the heart, kidneys, or lungs, and surround- 
ings which preclude proper sanitation and nursing, greatly 
lessen the probability of a favorable outcome. 

3. The presence or absence of complications. Any severe 
complication renders the prospect much less hopeful. Heart 
weakness, in particular, is of serious import. 

Treatment. — The treatment of typhoid fever resolves itself 
into four essentials, viz., 

1. Absolute rest. The patient must be put to bed under 
charge of a competent nurse and the slightest unnecessary 
muscular effort interdicted. The bed pan must be used, and 
even changes of posture must be accomplished with the aid of 
the attendant. 

2. Liquid diet. Sterilized milk, two to four pints in twenty- 
four hours, and given in divided doses every two hours, is the 
best food. If this fails to be digested, as evidenced by the 
appearance of small coagula in the stools, peptonize it or add 
lime water, or change to koumiss, buttermilk or junket. 
Gelatin, beef tea and gruel may be useful at times. Sterilized 
w r ater should be given freely. 

3. Sanitary precautions to prevent the spread of the disease. 
This includes disinfection of the excreta. The latter should 
be allowed to remain in contact for an hour with a pint of a 
1-1000 solution of corrosive sublimate, or of a solution of 
chloride of lime, six ounces to the gallon. 

4. Therapeutic measures adapted to the individual. These 
may be considered as applied to typhoid in general and also 
as demanded by special symptoms or complications. 

The pyrexia is best controlled by the use of external cold. 



32 INFECTIOUS DISEASES. 

A certain point, about 102.5° F., may be regarded as a maxi- 
mum, and elevation of the temperature beyond that point de- 
mands free sponging with cold water; and if the pyrexia 
persists, the use of the "cheese-cloth bath" or the cold pack. 
Hyperpyretic cases uncontrolled by these simple measures 
may be benefited by high colon flushes of cold water. The 
general cold bath, according to the method of Brand, must 
be used from the first days of the disease if at all. 

Medicines. — During the initial stage of the fever the reme- 
dies most frequently demanded by the general condition of the 
patient are bryonia and baptisia. Less often special remedies 
are demanded by certain symptoms, such as headache {bella- 
donna, spigelia, gelsemiiun) or general pains (rkus tox., etc.). 

With the advent of the second week the developing typhoid 
state generally demands rhus tox. At times a bad state of the 
mucous membrane will suggest baptisia or mercurius, and 
should either of these fail and the progress of the condition be 
evidenced by a red, raw tongue, with food badly borne, great 
thirst, and offensive watery stools, recourse may be had to 
cantharis, lacliesis (especially if there be a comatose state) or 
turpentine (tympanites and other abdominal symptoms). 

Catarrhal enteritis with mental apathy suggests phosphoric 
acid, while symptoms of gastric catarrh with constipation will 
be benefited by hydrastis. 

Nervous symptoms, if profound, require another class of 
medicines, chief of which are hyoscyamus (furious delirium), 
stramonium (cheerful delirium), and agaricus (delirium with 
tremor and rigidity). Muscular failure with great prostration 
and low delirium calls for hydrochloric acid, while the extreme 
typhoid state, with heart failure and general collapse, may 
suggest arsenic. 

Intestinal hemorrhage may be controlled by such remedies 
as liamamelis (sore feeling through the abdomen), turpentine 
(meteorism, flatulence, offensive stools, and possibly albumi- 
nuria), hydrastis (heavily coated tongue, etc.), and ipecac 
(griping colic below the navel). Should these fail and grave 



INFECTIOUS DISEASES. 33 

danger be apparent, give morphine sulphate, gr. \- \, hypo- 
dermatically. Subcutaneous or intra-venous injection of a 
quart or more of warm saline solution is advisable if there be 
great loss of blood. 

Tympanites may be controlled by care in diet, the appli- 
cation of cold to the abdomen, and a carefully selected gen- 
eral remedy. An extreme accumulation of gas may be relieved 
by the passage of a long rectal tube. 

Perforation is treated as peritonitis, and in the absence of 
possible surgical intervention, is usually fatal. A rising leuco- 
cyte count in the presence of suspicious symptoms, may be 
made the signal for abdominal section. 

Constipation should be relieved every second day by 
the use of an enema. 

Stimulants are indicated when the first sound of the heart 
weakens and the pulse becomes soft. Good brandy or whisky, 
four to eight ounces in twenty-four hours, is best. Strychnine 
sulph. y gr. Tnnnr» three to six times a day, may be required. 

Heart failure, if advancing in spite of symptomatic treat- 
ment and stimulation, demands the hypodermatic use of 
strychnine sulph., gr. -g-V - ¥o> spartein sulph., gr. \, agaricin, 
gr. yV, or camphorated oil (camphor, 3j in olive oil, 3j) in 
repeated doses of one drachm each. 

Convalescence may be regarded as established after the 
temperature has remained normal for two or three days. It 
is better to wait at least a week, however, before giving any 
solid food, and then but little at a time. Any rise in tempera- 
ture calls for an immediate return to liquid diet. Exercise 
must be attempted only as returning strength permits. 

TYPHUS FEVER. 

(Cerebral Typhus; Ship or Jail Fever.) 

Etiology. — Typhus fever is endemic in parts of Ireland, Eng- 
land, and Continental Europe, occasionally becoming epi- 
demic elsewhere. It is one of the most virulent of contagious 
3 



34 



INFECTIOUS DISEASES. 



diseases, sparing few who come in contact with it. The 
infection is transmitted from person to person and by fomites, 
but its " striking distance" is limited to about five feet, the 
virus being destroyed by the air. The specific cause, pre- 
sumably a micro-organism, has not been discovered. By pre- 
ference it attacks those whose resistance has been destroyed 
by bad hygiene, starvation, filth, and overcrowding. 

Pathology. — Typhus fever presents no distinctive lesion ex- 
cept its eruption. The general tissue changes are degenerative 




Fig. 2. — The Typical Temperature Curve of Typhus Fever 

Kalteyer.) 



(Salinger- 



in character and do not differ from those of typhoid fever and 
other acute infections in which toxemia is profound. 

Clinical Course. — After few, if any, prodromes, there is an 
abrupt onset of chills or chilliness, followed by a fever, head- 
ache, nausea, vomiting, muscular pains and profound prostra- 
tion. Within a day or two the temperature reaches 104° or 
105° F. The face is flushed and the eyes injected; and about 
the fourth day the eruption appears. Delirium develops 
rapidly. At first it is mild, but soon becomes muttering or 



INFECTIOUS DISEASES. 35 

■maniacal, and in the course of the second week it may merge 
into coma or coma vigil (unconsciousness with open eyes). 
The typhoid state, with tremor, subsultus tendinum, dry, 
brown tongue, albuminuria, and incontinence of urine and 
feces, becomes fully developed; often it is complicated with 
bronchitis or broncho pneumonia. The temperature remains 
high continuously, and the pulse is rapid (120-140) from the 
beginning. The heart grows steadily weaker until in many 
cases a fatal issue is reached. Should this not occur, however, 
the febrile period ends by crisis about the end of the second 
week, when often the patient falls into a refreshing sleep from 
which he awakens convalescent. 

The eruption appears from the third to the fifth day, and 
consists of dirty pink macules occurring on the covered por- 
tions of the body; these rapidly become petechial and do not 
disappear on pressure. Undeveloped spots give rise to a sub- 
cutaneous mottling, and the combined effect has been de- 
scribed asa " mulberry rash." 

Complications. — Hypostatic congestion of the lungs; catarrhal 
pneumonia, possibly ending in gangrene; nephritis, and sup- 
purative parotitis. 

Diagnosis. — Typhoid fever is differentiated by (1) a gradual 
onset; (2) a less abundant, non-petechial eruption, which ap- 
pears later in the disease; (3) the later development of ner- 
vous phenomena; and (4) the gradual termination. 

Cerebrospinal meningitis is marked \>y occipital headache, 
retraction of the head, hyperesthesia, and a tendency to 
opisthotonos and ocular palsies. 

Prognosis. — The mortality varies from 10 to 50 per cent, in 
different epidemics. It is necessary in each case to consider 
(1) the severity of the infection, (2) the personal factor, and 
(.3) the complications. 

Treatment. — Isolation. Absolute rest. Liquid food. The 
power of atmospheric air to destroy the infection suggests the 
need of free ventilation, or even treatment in the open air. 
The general management, including hydrotherapeutic and 



36 



INFECTIOUS DISEASES. 



medicinal measures, does not differ from that required by 
typhoid. 



RELAPSING FEVER. 

Etiology. — The exciting cause is a spirocheta {spirillum Ober- 
meieri), a slender motile spiral three to six times the diameter 
of a red blood corpuscle in length. It is found in the blood 
during a paroxysm, disappearing during the intermissions and 




Fig. 3.— The Temperature Chart of a Case of Relapsing Fever. (Salinger- 

Kalteyer. ) 

giving place to round, glistening bodies supposed to be spores. 

The disease is actively contagious, either through personal 
contact or by fomites. Overcrowding, filth, and starvation 
are predisposing factors, and epidemics often occur in connec- 
tion with those of typhus. 

Pathology. — There is no characteristic lesion. The spleen is 
enlarged and softened, and may rupture. Degenerative 
changes occur in the liver, kidneys, and heart. 



INFECTIOUS DISEASES. 37 

Clinical Course. — The attack begins abruptly with a chill, fol- 
lowed by high fever (104°-105°) which remains continuous. 
The patient suffers with headache, severe general pains, and 
prostration, but the mind remains clear. Jaundice is common. 
About the fifth day the temperature falls suddenly to or below 
normal, and this crisis may be accompanied by severe sweat- 
ing, exhausting diarrhea, collapsic symptoms, or hemorrhages 
from stomach, bowels, or kidneys. 

After an intermission of five or six days there is a second 
but often milder paroxysm of the same duration. Generally 
convalescence then ensues, but the paroxysm may recur as 
often as five times. 

Complications. — Hyperpyrexia; catarrhal pneumonia; neph- 
ritis. 

Sequelae. — Slow convalescence, often with muscular and joint 
pains and lymphatic swellings. Post-febrile ophthalmia, with 
possible loss of sight. 

Diagnosis. — Any doubt will be removed by finding the spiro- 
cheta in the blood. 

Prognosis. — Death, though not common (1-4%), may occur 
from cardiac thrombi or emboli, or from other complications. 

Treatment. — The general management should be that of any 
infectious disease. The remedies indicated during the stage 
of invasion include aconite, bryonia, and veratrum viride ; 
while the fully developed disease may require bryonia, rhus 
tox., baptisia, cimicifuga, or cupatoriiim'perfoliatum. 

DENGUE. 

(Dandy or Break-bone Fever. ) 

Etiology. — Dengue occurs epidemically in the tropics and 
sub-tropics during the summer season, frost dissipating the 
infection. It is contagious, but the specific organism has not 
been isolated. 

Pathology. — The disease is essentially a toxemia accompanied 



38 INFECTIOUS DISEASES. 

by an inflammation of serous structures (joints and tendon 
sheaths). No characteristic lesions have been found. 
Symptoms. — The essential features of dengue are: 

1. Fever, (a) An initial paroxysm lasting three or four 
days, followed by 

(&) A remission of two or three days, and 
(c) A terminal paroxysm, shorter and less severe than the 
first. 

2. Severe muscular and articular pains. During the febrile 
paroxysm the muscles are tender and the joints are red, 
swollen and painful. 

3. A rash. This is not distinctive: there may be an initial 
rash of scarlatinal character, which disappears quickly, and is 
followed on the fourth and fifth day by an eruption which may 
be erythematous, urticarial or herpetic. Often desquamation 
ensues. 

Clinical Course. — The disease begins abruptly with a slight 
chill followed by fever (102°-107° F.), and headache, back- 
ache, and severe pains in muscles and joints. Prostration is 
marked and a scarlatina-like rash may be present. At the end 
of three to five days a crisis, often accompanied by diarrhea or 
sweating, occurs, and the general symptoms disappear, leav- 
ing the patient stiff and sore. At this time various eruptions 
appear. In two or three days the characteristic symptoms 
reappear, but this febrile paroxysm is milder and shorter 
than the first, and is followed by slow convalescence. 

Less commonly the attack is accompanied by hemorrhages 
from the mucous membranes, inflammation of the respiratory 
tract, and lymphatic swellings. 

Diagnosis. — Rheumatic fever runs a dissimilar course and 
is usually without eruption. 

In influenza the temperature is not remittent, the joints 
are rarely involved, and serious complications are frequent. 

Yellow fever may be distinguished by the occurrence of 



INFECTIOUS DISEASES. 39 

jaundice, black vomit, albuminuria and severe nervous phe- 
nomena. 

Prognosis. — Favorable; death is rare. 

Treatment. — Rest in bed, generous fever diet, and such reme- 
dies as aconite, bryonia, gelseminm, rhus tox, eupatorium and 
arsenic. 

MILIARY FEVER. 

( Sweating sickness. ) 

Etiology. — An infectious disease, without definite pathologic 
lesion and with an unknown specific cause, which occurs in 
rare epidemics in districts of limited area. Usually it prevails 
in spring and summer and attacks a large percentage of the 
population in the invaded district. 

Symptoms. — There are a few prodromal symptoms: head- 
ache, malaise and prostration. Then suddenly the patient is 
seized with moderate fever, profuse sweating and severe pain 
in the epigastrium. On the third or fourth day an eruption 
appears. It consists of small red spots, varying in shape and 
size, in the centre of each of which a vesicle forms in a few 
hours. The contents of the latter become opaque, and in the 
course of two or three days it dries up, forming a crust 
which falls off and leaves a normal surface. In severe cases 
profound nervous symptoms and asthenia may develop. 

Diagnosis. — Rheumatism may be distinguished by its swollen 
joints; the eruption of measles is not vesicular; and malaria 
has a periodic pyrexia. Knowledge of the prevalence of an 
epidemic renders diagnosis easy. 

Prognosis. — This varies with the character of the epidemic. 
The average death rate is about 10 per cent. 

Treatment should be conducted as in other acute infections, 
therapeutic measures being adapted to symptomatic demands. 



40 INFECTIOUS DISEASES. 

INFLUENZA. 

(I>a Grippe, Catarrhal Fever.) 

Etiology. — This disease occurs in great epidemics, which 
spread over the world with almost inconceivable rapidity. 
Sporadic cases occur at other times. It is mildly contagious, 
but on account of its rapid spread the method of infection is 
difficult to explain. Sex, age, condition and climate have no 
influence. The exciting cause is the bacillus of Pfeiffer, a 
minute rod found in the catarrhal discharges. 

Pathology. — There are no characteristic lesions, the disease 
being essentially a profound toxemia. 

Symptoms. — There is a sudden onset, usually with high fever 
which lasts for several days and is accompanied by profound 
prostration and great pain in the head, back, and extremities. 
As a rule the attack is marked by severe catarrhal conditions 
of the respiratory or gastro-intestinal tract. 

Clinical Types. — The varying localization of the disease has 
led to its classification into: 

1. The Catarrhal Variety. — This is distinguished by catar- 
rhal inflammation of the respiratory or gastro-intestinal tract. 

2. The Nervous Variety. — This form is characterized by 
delirium and hyperesthesia of the special senses. In addition 
a typhoid type may develop, in which the typhoid state is ad- 
ded to nervous and gastro-intestinal symptoms. 

Complications.— These are extremely common and may involve 
the respiratory tract (catarrhal or croupous pneumonia, 
pleurisy, empyema), the circulatory system (endocarditis, 
pericarditis, heart failure), or the nervous system (neuralgia, 
neuritis, insanity). 

Diagnosis. — The association of catarrhal symptoms with a 
profound prostration altogether out of proportion to the 
severity of the other symptoms renders diagnosis easy in most 
cases. Doubt may be removed by staining a cover-glass 
specimen of the respiratory secretion with Ziehl's carbol- 



INFECTIOUS DISEASES. 41 

fuchsin or Loeffler's methylene blue, when the characteristic 
short, thick rods will be revealed. Typhoid fever may be 
distinguished by the Widal reaction. 

Prognosis. — Influenza is rarely fatal except through complica- 
tions, upon recognition of which the prognosis must be based. 

Treatment. — Absolute rest in bed with a nourishing liquid 
diet. Stimulants are often necessary. 

The symptoms at the onset are usually met by gelsemium y 
though sthenic cases may require aconite. Bronchial symp- 
toms associated with intense pain in the extremities are 
relieved by bryonia. Great restlessness and pain suggest 
rhus tox., while eupatorium is useful in cases in which inflam- 
mation of the upper respiratory tract is accompanied by 
marked pain and soreness of the entire body. Gastro-intes- 
tinal symptoms may demand such remedies as ipecac, arsenic, 
and cuprum arsen. 

Complications should be treated as independent conditions. 

YELLOW FEVER. 

Etiology. — Yellow fever is endemic in the West Indies, whence 
occasionally it spreads along lines of travel to surrounding 
countries, particularly the southern United States. The dis- 
ease is not directly contagious. The specific germ is probably 
conveyed from one infected individual to another by mosquitoes 
rather than by fomites. Thorough disinfection and quarantine 
are effective safeguards. 

Pathology. — The invasion of the organism leads to: 

1. Rapid blood decomposition. The red corpuscles are dis- 
organized, hemoglobin is set free, and the blood becomes 
dark and its coagulability diminished. 

2. Tissue degenerations. The toxemia leads to granular 
and fatty changes, and occasionally hemorrhagic infarcts, in 
the liver, kidneys, and heart. The gastro-intestinal mucosa 
becomes inflamed and eroded. 



42 INFECTIOUS DISEASES. 

3. Jaundice. Often the skin becomes yellow, hence the 
name of the disease. In the early stages this may be slight, 
but later the patient's skin assumes a saffron-color. 

Symptoms. — 1. The stage of invasion is marked by a chill, a 
rapid rise of temperature, and pain in the head, back, and limbs. 
The face is flushed and the eyes suffused. The epigastrium 
is tender, the stomach is irritable, and vomiting occurs fre- 
quently. The temperature remains high for about three days, 
then falls to nearly normal. 

2. The "stage of calm" the remission which now occurs, 
may initiate convalescence in mild cases. All the symptoms 
moderate, but as a rule, in a day or two, a third stage super- 
venes, viz., 

3. The stage of relapse. The temperature rises rapidly, 
jaundice develops, the symptoms become aggravated, and as. 
a result of kidney involvement a uremic condition is added. 
There is intense gastric irritability and often "black vomit," 
due to the presence of altered blood in the vomitus. The 
urine is scanty, albuminous, and may contain hyalin casts and 
blood; complete suppression may occur. Cerebral symptoms 
develop, varying from mild delirium to profound coma. The 
prostration may merge into the typhoid state, or collapse may 
ensue. Hemorrhages beneath the skin and from the mucous 
membranes are common. The duration of this stage varies. 
Death may occur from collapse, hemorrhage, or uremia. 

Diagnosis. — As a rule, the symptoms of yellow fever are so 
unmistakable that an error in diagnosis is impossible. A 
malarial fever can be excluded by the absence of the parasite 
from the blood. 

Prognosis. — The mortality varies from 10 to 80 per cent., 
according to the epidemic. Hemorrhages, anuria, and cere- 
bral symptoms are of grave significance. 

Treatment. — Absolute rest. Little or no food during the 
period of invasion; later, light liquid food, and rectal feeding 
if necessary. Increasing prostration requires alcoholic stimu- 
lants. 



INFECTIOUS DISEASES. 43 

Of remedies, in the earl} 7 stage aconite, belladonna, and 
camphor have proved valuable. Later, gastric symptoms ma} 7 
require bryonia, or incessant vomiting may demand ipecac or 
argentum nit. The profound toxemia of the third stage calls 
for such remedies as arsenic, lachesis, and crotahis. Cerebral 
symptoms suggest belladonna, Jiyoscyamus, and opium; and 
the urinary symptoms are met by cantharis. 



DYSENTERY. 

Etiology. — Inflammations of the colon, for which dysentery 
is a generic term, are common in the tropics, with occasional 
sporadic or epidemic outbreaks in temperate regions. Their 
exciting causes, presumably microbic and supposed to be con- 
veyed in drinking water, are not determined definitely. The 
amoeba coli is credited with causing the tropical form. 

The predisposing factors include a tropical climate, late 
summer and autumn, unhygienic surroundings, and dietetic 
transgressions. 

Pathology. — The anatomical lesions permit a division into 
three acute forms, any of which may merge into a chronic 
form. 

1. Catarrhal dysentery. The mucous membrane of the colon 
is swollen and congested and the solitary glands are enlarged 
and may ulcerate. 

2. Amoebic {tropical) dysentery. The mucous membrane is 
edematous, with localized areas of cellular infiltration which 
become necrotic and slough off, leaving irregular ulcers. 
These undermine the mucosa, extending at times down to the 
serous coat; and they contain amoebae in large numbers. 
Hepatic abscess is a common complication, and it may rupture 
into pleura or lung. A diphtheritic inflammation may be 
associated. 

3. Diphtheritic dysentery. The colon is swollen and covered 
with a croupous exudate, which sloughs away and leaves 
large irregular ulcers. 



44 INFECTIOUS DISEASES. 

4. Chronic dysentery. As a result of persistent inflam- 
matory changes the walls become thickened and often ulcer- 
ated. Healing by cicatrization may lead to stricture of the 
intestine. 

Symptoms. — After several days of diarrhea, which gradually 
becomes severe and painful, the stools lose their fecal char- 
acter and instead consist largely of blood, pus and mucus. At 
the same time persistent and severe rectal tenesmus (bearing 
down) and tormina (abdominal griping) occur. There is 
moderate fever, considerable prostration, and in the diph- 
theritic form a typhoid state may develop. Death may occur 
from exhaustion or as the result of some complication, such 
as peritonitis or abscess of the liver. The duration of an 
acute attack varies from one to eight weeks, according to its 
severity. 

Diagnosis.— Dysentery differs from ordinary diarrhea in the 
occurrence of mucoid and bloody stools associated with great 
tenesmus. Local rectal conditions may give rise to loose and 
bloody stools, but the history together with a local examina- 
tion will reveal the true nature of the process. 

Prognosis. — In ordinary catarrhal cases the prognosis is 
favorable, and in the tropical cases it is guardedly so, but in 
the diphtheritic cases the outcome is doubtful. In epidemics 
the mortality varies from 10 to 70 per cent. 

Treatment. — Absolute rest in bed, with use of the bed pan, 
•careful disinfection of the excreta, personal cleanliness, liquid 
diet, and stimulants when needed. Irrigations of the bowel 
with large quantities of boiled water, plain or containing ten 
grains of boric acid to the ounce, repeated every six to twelve 
hours, are advisable. Hot fomentations may be applied to 
the abdomen to relieve pain. 

Of remedies, mercurius dulcis may be administered in mild 
attacks, but mercjirius corr. is pre-eminently useful in tropical 
cases. In the severe forms cantJiaris and arsenic are fre- 
quently indicated also. Severe tenesmus may be relieved by 
belladonna, aloes or mix vomica ; while colicky abdominal 
pain suggests the use of ipecac, colocyntli or cuprum ars. 



INFECTIOUS DISEASES. 45 

Care in diet and exercise during convalescence is imperative,. 
lest the disease pass into a chronic form. 

THE MALARIAL FEVERS. 

Etiology. — The specific cause is a parasite ^Plasmodium ma- 
laria;, hemosporidia) which is conveyed to man by a mosquito 
{anopheles). The disease prevails in all parts of the world, 
but particularly in tropical and other warm climates. Low, 
damp and marshy regions are especially apt to be malarial. 

Pathology. — The organisms appear in the blood as small, 
whitish protoplasmic masses of varying shape (discoid, an- 
nular, etc.), possessing rapid amoeboid motion. Within a red 
corpuscle this small colorless body appears, and as it grows 
minute yellowish granules begin to develop. The corpuscle 
becomes somewhat expanded and loses its color, while the 
amoeboid movements of the organism grow less and the amount 
of pigment increases and darkens. Finally the pigmentary 
granules collect into a clump, radial striations appear, and at 
last, the surrounding red corpuscle having become almost in- 
distinguishable, the capsule ruptures suddenly and the fifteen 
or twenty segments, each a spore, escape into the blood. 
These spores invade fresh corpuscles, in which this cycle of 
development is repeated. The typical febrile paroxysm in the 
patient occurs at the moment of segmentation. 

Several varieties of the organism, varying in form, cycle of 
development, and clinical manifestations, are recognized, viz., 

I. The Parasite of Tertian Fever. This organism, which 
has just been described, completes its life cycle in about forty- 
eight hours. 

II. The Parasite of Quartan Fever. With the exception of 
a period of development extending over seventy-two hours, 
this organism differs from the tertian only in minor particulars, 
being smaller, less active, more refractive and showing a 
smaller number of segments. 

III. The Parasite of Estivo-autumnal Fever. This is less 
apt to pass through the cycle of development in groups; organ- 






46 INFECTIOUS DISEASES. 

isms in various stages coexist, and large ovoid and crescentic 
bodies are also seen. The precise period of time occupied by 
the life cycle of this parasite has not been determined. In 
connection with this and other varieties, extra-corpuscular 
forms, some with flagellar, have been described. 

By their action these organisms destroy the red corpuscles, 
liberating the pigment (melanemid) and ultimately cause ex- 
treme anemia. The spleen becomes greatly swollen (ague- 
cake), the liver moderately enlarged, and all the organs are 
discolored by the pigment. 

Symptoms. — The malarial paroxysm, which occurs in the 
regularly intermittent forms, may be divided into three char- 
acteristic stages, viz. : 

1. The chill. 

2. The fever. 

3. The sweat. 

Prodromes are often slight and may be absent. If they 
occur, they consist of slight general lassitude and headache, and 
often yawning and stretching. There may be nausea and vomit- 
ing. Chilly sensations follow rapidly, and soon the patient is in 
the midst of a severe shaking chill. Usually this lasts for less 
than half an hour, during which period the temperature is ris- 
ing steadily. Then the chilliness gradually diminishes and is 
succeeded by a sensation of intense heat. The skin, pre- 
viously pale and cool, becomes flushed, hot and dry, the 
temperature may reach 106° or 107°; and aching in the head, 
back, and limbs becomes intense. After some hours of intense 
fever, sweating begins and is soon profuse, and then the tem- 
perature falls rapidly and all the symptoms are relieved. Dur- 
ing the intermission which ensues the patient may feel quite 
well; but at the end of the period the attack is repeated just 
as before. 

Types of Fever. — Malarial fevers are divided, according to the 
causative organism and the resulting periodicity of the parox- 
ysms, into three main forms, viz. : 



INFECTIOUS DISEASES. 



47 



The regular intermittent forms: 

1. Tertian Fever. This includes (a) tertian paroxysms; and 
($) double tertian fevers, or a quotidian of tertian origin. 

2. Quartan Fever. This includes the {a) quartan, (/;) double 
quartan, and (c) triple quartan or quotidian of quartan origin. 

The irregular form: 

3. Estivo-antinnnal fever, usually a tertian of malignant 
type, but possibly a quotidian or irregular continued fever. To 
this group belong all the pernicious and many of the tropical 
fevers. 



April 



Hour 



Hour 



Temp. 
105 



104 
103 
102 
101 
100 
99 



£ 



w 



m. 



Vi 



Temp 
C. 



40 



39 



3T 



m 



Fig. 4. — The Temperature chart of a Tertian Malarial Fever. (Salinger- 

KalteyeO 

In addition to these, certain malarial phenomena have re- 
ceived special designations. 

Pernicious or Malignant Malaria, rare in temperate climates but 
common in the tropics, is due to the abundance of parasites, 
their rapid multiplication and their malignancy, and to the 
special involvement of certain vital organs (central nervous 
system, gastro-intestinal tract, etc.). In consequence of the 



48 



INFECTIOUS DISEASES. 



latter fact, the pernicious paroxysm varies greatly in its clini- 
cal character. It may begin with violent delirium, which 
sometimes develops into mania or convulsions, occasionally 
into hemiplegia or symptoms of bulbar paralysis. More often 
the initial delirium merges into deep and often fatal coma. In 
some cases the symptoms simulate the algid stage of Asiatic 
cholera, while other cases are distinguished by hemorrhages 
(epistaxis, hemoptysis, hematemesis, and petechias) or by 
marked jaundice. 

Malarial Hemoglobinuria occurs in connection with some severe 
malarial paroxysms, as the result of destruction of the red 
corpuscles by the parasites, together, perhaps, with the toxic 
action of quinine. The urine becomes an intense brownish- 



Jime| 2 9 



TZK 



Hour 



Hour 



Temp. 

105 
104 
108 
102 
101 
100 



JL 



P 



25 



tag 



E2 



40 



37 



Fig. 5. — Temperature Chart of an Estivo-Autumna Malarial Fever. 
( Salinger- Kalteyer . ) 

black in color, and on standing deposits an abundant sedi- 
ment of mucus, bladder and renal epithelium, pigment, and 
casts. Nephritis follows invariably. 

Combined infections with different varieties of the parasite may 
occur. A double quartan infection, two groups of quartan 
organisms reaching maturity on successive days, occasions 
paroxysms on two days followed by one day of intermission. 
A triple quartan, three sets of parasites maturing on successive 



INFECTIOUS DISEASES. 49 

days, causes quotidian paroxysms; or the latter may be evi- 
dence of a double tertian, two groups of the latter parasites 
maturing on alternate days. 

Malarial Cachexia, resulting from repeated or long-continued 
attacks, is a condition of grave anemia. The skin becomes sal- 
low, and there are severe headaches or neuralgias, marked 
dyspnea, gastro-intestinal disturbances and edema of the ex- 
tremities. A post-malarial anemia, resulting from the ex- 
tensive blood destruction, but less severe in type, is common 
also. 

Complications. — The malarial attack may be accompanied or 
followed by pneumonia, pleurisy, tuberculosis, nephritis and 
typhoid fever. 

Diagnosis. — The diagnosis of any form of malaria becomes 
positive only upon the demonstration of the Plasmodium in 
the blood. For this purpose a drop of fresh blood may be 
examined under the microscope at the bed side or the drop 
may be spread upon a slide, allowed to dry in the air, and sub- 
sequently hardened in equal parts of alcohol and ether for 
half an hour and then stained with hematoxylin and eosin. 
Careful systematic search under a 1-12 inch lens will reveal 
the characteristic bodies within the red corpuscles. 

In almost all conditions which simulate malaria a well- 
marked leucocytosis occurs. In consequence an increase in 
the number of leucocytes is strong evidence against the ex- 
istence of an uncomplicated malarial fever. 

The chronic malarial cachexia may be mistaken for primary 
or secondary anemia, leucocytJiemia, or pseudo-leucocythemia. 
In the absence of the parasite or of pigment in the blood, the 
diagnosis, except in leukemia, is difficult; but the history, 
together with the response of the patient to treatment, will 
ultimately distinguish the malarial case. 

Typhoid fever is distinguished from malaria by its tempera- 
ture curve, gastro-intestinal symptoms, and eruption. Tuber- 
culosis is readily distinguished by its physical signs in associa- 
tion with the bacilli in the sputum. Internal suppurations 
4 



50 INFECTIOUS DISEASES. 

offer a history of previous disease, together with localized pain 
and physical signs. Ulcerative endocarditis may be excluded 
by auscultation over the heart. The intermittent fever of 
cholelithiasis is irregular, is associated with colic or pain in 
the hepatic region and jaundice, and ceases soon after the 
passage of the stone. 

Prognosis. — Under appropriate treatment the outlook in the 
regularly intermittent fevers is good, and this statement 
applies, though less strongly, to the estivo-autumnal infection. 
Malarial hemoglobinuria is of grave portent. The malarial 
cachexia often requires for its control a change in the patient's 
environment. 

Treatment. — If possible, remove the patient to a non-malari- 
ous district. Place him at rest in a room or bed protected by 
mosquito netting until the disease is controlled. 

Quinine sulphate or bisulphate, in a dose of from ten to 
fifteen grains three or four hours before the paroxysms, acts 
as a direct parasiticide, destroying the organisms in the blood. 
It may then be continued in decreased dosage, the larger 
quantity being given only prior to an anticipated seizure. 

Methylene blue, given in capsules containing one grain from 
three to six times daily, has a similar action and is especially 
recommended for the hemoglobinuria cases. 

Pernicious paroxysms may be met by the intravenous injec- 
tion of a solution of quinine hydrochlorate, gr. xv, and sodium 
chloride, gr. xij, in tepid distilled water, 3iiss; or a similar 
solution may be used in larger doses hypodermatically. 

In acute cases nausea may be controlled by ipecac, head- 
ache by belladonna, and a profound chill may suggest the use 
of camphor, arsenic, or veratrum alb. 

The estivo-autumnal fever, if not controlled by quinine, may 
be benefited by the use of such remedies as arsenic, quinine 
arsenite, arsenic iodide, and bryonia. The cachexia should 
be combated by attention to general hygiene and nutrition, 
and the use of the remedies just mentioned, or possibly of iron 
preparations {ferrum ars., ferrum met., ferrum phos.). 



INFECTIOUS DISEASES. 51 

RHEUMATIC FEVER. 

(Inflammatory Rheumatism; Acute Articular Rheumatism. ) 

Etiology.— The exciting cause is a micrococcus, the infective 
agent entering the body through the tonsils, through wounds, 
etc. Among the more important predisposing causes are 
heredity, previous attacks, and exposure to wet and cold. 

Pathology. — The articular changes consist of inflammation of 
the synovial membranes and ligaments, effusion into the joints, 
and inflammation and edema of the peri-articular structures, 
including tendon-sheaths, bursae, muscles and fascia. The 
cartilages are roughened and may become eroded. The pro- 
cess usually terminates by resolution, but organization of 
plastic lymph may lead to fibro-cartilaginous ankylosis of the 
joint, and yet more rarely suppuration ensues. 

Symptoms. — The invasion is usually abrupt, with a rise of 
temperature, sometimes preceded by a chill, and pain in cer- 
tain joints. 

1. The joints and surrounding structures are swollen, red, 
and painful. The medium-sized joints (knee, ankle, wrist) 
are first involved; the larger and smaller joints are attacked 
later. They are not affected simultaneously, the process 
changing from one joint to another from time to time; but 
anywhere from one to a dozen articulations may be inflamed 
at the same time. 

2. The skin is covered with a copious, sour-smelling per- 
spiration. Sudamina, erythema, urticaria, or purpura (pe- 
liosis rlieumatica) may appear; and small subcutaneous 
nodosities (rheumatic nodule 's), which are firm, slightly mov- 
able, and painless, may develop in the tendons and fascia. 

3. The fever varies in height according to the severity of 
the infection (101-105°), and hyperpyrexia (106-108°) occurs 
in some severe, generally fatal, cases. Restlessness, delirium, 
coma, and convulsions may accompany the febrile state. 

4. The heart is quickened in its action, the pulse-rate reach- 



52 INFECTIOUS DISEASES. 

ing 100 or more, and there is a notable tendency to the de- 
velopment of local infection in the form of endo-, peri- or 
myo-carditis. In children these lesions may occur in the 
presence of few if any articular manifestations. 

5. Blood changes are marked, the red cells becoming greatly 
reduced in number, with a corresponding loss of hemoglobin, 
and the leucocytes becoming increased, even up to 39,000.. 
Fibrin and lactic acid are in excess. 

Course.— Indefinite. The duration of the disease may vary 
from a few days to many weeks, and it may merge into a sub- 
acute form. 

Complications. — Endocarditis (very common), pericarditis, 
myocarditis, hyperpyrexia, pleurisy, pneumonia, chorea, iritis,, 
meningitis. 

Diagnosis. — Gout occurs in older persons, affects small joints, 
the fever is not high, and there are no acid sweats. 

Osteomyelitis gives a history of long-continued pain, worse 
at night; it affects generally but one joint and presents mod- 
erate fever and no acid sweats. 

Septic arthritis occurs in connection with some septic pro- 
cess elsewhere, its onset is slower, it has no acid sweats, and 
tends to end in suppuration. 

Prognosis. — While recovery is the rule, complications may 
render the outlook grave; and the persistence of the valvular 
heart disease induced by endocarditis may seriously affect the 
future health of the patient. 

Treatment. — Place the patient at absolute rest in bed between 
blankets, and wrap the joints in absorbent cotton. Cleanse 
with warm water and soap daily, nourish with semi-liquid food, 
and allow plain, aerated, or acidulated water freely. Examine 
the heart daily for signs of its involvement. Aconite may 
be given early in restless, apprehensive patients with active 
fever. As the disease progresses, bryonia is demanded by 
pains which the slightest motion aggravates, and which 
may be accompanied by thirst, gastric irritability, constipa- 
tion, etc. ; pericarditis, pleurisy, or pneumonia is apt to afford 



INFECTIOUS DISEASES. 53 

additional indications for its use. Rhus tox. is required in 
cases so restless that the patient must move in spite of the 
pain, and the latter may be general, involving back and limbs 
as well as joints. Pulsatilla is recommended for cases in 
which the disease wanders from joint to joint, or especially 
affects the knees; merairitts, when the patient sweats freely, 
has aggravated pain at night, and presents symptoms of 
gastro-intestinal catarrh. Belladonna is suggested by red, 
throbbing joints and characteristic general symptoms; caulo- 
phyllum, by involvement of small joints, and cimicifuga and 
Phytolacca by involvement of the trunk muscles. In typical 
cases a solution of colchicine, one grain to the ounce of alcohol, 
may be given in doses of 3-5 drops every two to four hours, 
and the effect is often magical. Sodium salicylate, in doses of 
5-15 grains every two hours until pain is relieved and then in 
lessened dosage, is widely used. In every case the patient 
must remain at rest, carefully protected from the slightest 
exposure, for some days after every symptom has disappeared. 

CEREBROSPINAL FEVER. 

( Epidemic Cerebro-spinal Meningitis, Spotted Fever. ) 

Etiology.— The disease may be epidemic or sporadic. The 
exciting cause is probably the meningococcus intracellularis. 
Cold weather and bad hygiene favor its development. 

Pathology. — The disease process begins as a congestion of 
the cerebro-spinal membranes, followed by the appearance of 
an exudate that is first serous and then purulent. The 
cortex and the nerve sheaths become involved in the inflam- 
matory process; while the toxemia causes degenerative changes 
in the viscera. 

Symptoms. — The onset is sudden, and is accompanied by chill, 
fever, prostration, headache and general pain. Vomiting may 
occur early or late and is often obstinate. More suggestive of 
the nature of the disease, however, is the severe headache with 
stiffness of the neck (from irritation of the upper cervical 
nerve roots). The symptoms grow worse rapidly, and de- 



54 INFECTIOUS DISEASES. 

lirium, and in severe cases coma, supervenes. In connection 
with the mental changes there may be signs due to the involve- 
ment of certain regions. Thus, pressure upon the cranial nerves 
may produce strabismus, nystagmus, ptosis, pupillary disturb- 
ances, optic neuritis with destructive changes in the eye, tris- 
mus and deafness. Pressure on the spinal nerves causes intense 
cutaneous hyperesthesia, stiffness and twitching of muscles, 
and occasionally swollen and painful joints. Opisthotonos, 
with constipation and retention of urine, may ensue. Death 
may occur within a few days. 

The temperature is irregular; leucocytosis is marked; and 
various atypical eruptions appear (herpes, erythema, urticaria, 
petechia). The course of the disease varies from one to 
many weeks. 

Complications and Sequelae.— Pneumonia (croupous or catar- 
rhal), pericarditis, endocarditis and pleurisy occur as com- 
plications. The destructive changes in the nervous tissues 
may lead to incurable headaches, mental enfeeblement, pa- 
ralyses, blindness, and deafness. 

Diagnosis. — The coincidence of headache, vomiting, nuchal 
rigidity and hyperesthesia of the entire nervous system strongly 
suggests cerebro-spinal meningitis. It may be necessary to 
exclude typhoid fever (gradual onset, with absence of herpes 
and of leucocytosis), pneumonia (physical signs and sputum), 
abscess of the brain (localized symptoms, no rigidity or hy- 
peresthesia), and tubercular meningitis (tuberculosis else- 
where, gradual onset, basal symptoms). 

Kernigs sign, said to be pathognomonic of cerebro-spinal 
meningitis, consists of a flexure contraction of the knee-joint, 
which in the sitting posture cannot without violence be 
straightened beyond 135° with the thigh, but which is easily 
straightened when the patient is erect or recumbent. 

A question as to the causative organism may rarely render 
lumbar puncture advisable. A long needle is passed a little to 
one side of the median line between the third and fourth 
lumbar vertebrae in adults, or between the fourth and fifth in 



INFECTIOUS DISEASES. 55 

children. The escaping fluid may be examined microscopi- 
cally and in cultures for the meningococcus intracellularis, the 
tubercle bacillus, etc. 

Prognosis. — The outlook is bad but not hopeless. The mor- 
tality varies from 20 to 75%. Severe cerebral symptoms 
render the prognosis grave. 

Treatment. — Rest and quiet in a somewhat darkened room, 
and a nutritious diet, liquid during the height of the disease, 
but semi-solid (rice, eggs, milk toast) as soon as convalescence 
begins. Stimulants are frequently required. 

For the early inflammatory symptoms, belladonna, bryonia, 
gelsemium, and veratrum viride are recommended. For the 
fully developed case cuprum acet. (marked cerebral symp- 
toms), or cicuta (predominating spinal symptoms) is to be 
preferred. Cerebral cases with coma may derive benefit from 
the use of apis, opium, or Jielleborus. A typhoid state will 
suggest the administration of arsenic, rJius tox., baptisia, 
crotalus, or lacJiesis. Actea is recommended for pains and 
spasms continuing after the acute symptoms have subsided. 

PNEUMONIC FEVER. 

(Croupous Pneumonia, Lobar Pneumonia.) 

Etiology. — The exciting cause is a bacterium, generally the 
pneumococcus (micrococcus lanceolatus), but possibly at 
times other organisms, including the bacillus pyogenes, the in- 
fluenza bacillus, and Friedlander's bacillus. 

Predisposing factors, which tend to lessen resistance to in- 
fection, are exposure to cold, the extremes of life, traumatism, 
and prior attacks of the disease. 

Symptoms. — The onset is sudden, and is generally attended by 
chill, high fever, pain in the side, and cough. The respirations 
become very rapid (40-80 per minute) and out of proportion to 
the pulse rate. Dyspnea may be marked. The face is flushed. 
The sputum is "rusty " or blood stained; less often, it is dark 
like prune juice. The gastro-intestinal system is deranged, the 



56 



INFECTIOUS DISEASES. 



spleen is enlarged, chlorides disappear from the urine, and 
there is a marked leucocytosis. Herpes appear upon the lips. 
Headache is common, and patients suffering from typhoid, 
nephritis or alcoholism may become delirious. The fever is 
continued for from three to fourteen days, and then terminates 
by crisis in most cases, resolution and convalescence ensuing. 
Resolution may, however, be delayed for weeks, the temper- 
ature declining gradually. 

In children pneumonia is frequently ushered in by convul- 
sions, followed by delirium and stupor. In the aged it may 
develop insidiously, with little fever and few symptoms ex- 
cept profound prostration. Cough may be absent in young or 
old. 




Fig. 6. — Chart Showing the Temperature Range in a Case of Pneumonic 
Fever. (Salinger-Kalteyer.) 

Pathology.— The process consists of a fibrinous exudation, 
with subsequent coagulation, into the alveoli of one or more 
lobes of the lung. Three stages are distinguished, viz., 

1. The stage of congestion. The portion of lung involved is 
intensely congested, dark red in color, heavier than normal, 
and from its cut surface frothy, blood-stained serum exudes; 
but since the air cells are not yet occluded, it crepitates on 
pressure and a fragment will float in water. Microscopically, 



INFECTIOUS DISEASES. 57 

the capillaries of the alveolar walls appear distended with 
blood, and the air cells contain exfoliated epithelial cells 
and blood corpuscles. 

2. The stage of consolidation. The tissue becomes solid 
and a mottled reddish brown in color, resembling liver tissue 
{red hepatization). It tears easily, and since it has become 
airless it no longer crepitates and will sink in water. Micro- 
scopically, the air cells appear distended and packed with 
clotted fibrin in whose meshes are held red blood corpuscles, 
leucocytes, epithelial cells and micro-organisms. 

3. The stage of resolution or diffuse suppuration. The red 
color gives place to gray {gray 1iepatizatio?i), this being due 
to the pressure of the exudate, the destruction of the red cor- 
puscles and the appearance of many leucocytes. Resolution 
begins in spots, in which fatty degeneration and liquefaction 
of the exudate occurs and is followed by its absorption or 
expectoration. In unfavorable cases, however, the lung may 
become infiltrated with pus, with consequent abscess or 
gangrene. 

Pleurisy, localized over the affected lung, is the rule (pleuro- 
pneumonia). The toxemia accompanying the local lesion, 
sometimes profound, leads to degenerative changes in the 
heart and other viscera. In addition, complicating lesions 
may occur as the result of infection of other organs (peri- 
carditis, endocarditis, meningitis). 

Physical Signs. — First stage (congestion) : tympanitic, slightly 
dull note over the affected (usually lower) lobe; crepitant 
rales. 

Second stage (consolidation): complete dulness; bronchial 
breathing; increased vocal fremitus. 

Third stage (resolution): the dulness gradually clears up, 
the bronchial breathing becoming vesicular, with numerous 
moist rales. 

Diagnosis. — The sudden onset, the characteristic sputum and 
the presence of leucocytosis, in connection with the physical 
signs, render diagnosis easy in most cases. The frequent 



58 INFECTIOUS DISEASES. 

occurrence of pneumonia late in the course of chronic diseases 
(diabetes, nephritis, etc.), without marked symptoms, sug- 
gests the need of careful physical exploration of the chest in 
all doubtful cases. 

Pleurisy lacks the abrupt onset, the peculiar sputum, and 
the change in the pulse-respiration ratio. In pleurisy vocal 
fremitus and resonance are diminished, the breath sounds 
are distant, and the upper line of dulness changes with the 
patient's posture. 

Pulmonary edema presents neither chill, fever, nor pain; the 
sputum is watery, and auscultation reveals moist rales over the 
entire area of both lungs. 

Pneumonic phthisis may be distinguished by irregular fever 
continued beyond the usual period of a pneumonia, and by a 
consolidation which begins more often at the apex than the 
base, and which subsequently presents signs of softening and 
excavation. It is accompanied by increasingly grave symp- 
toms, and by tubercle bacilli in the sputum. 

Typhoid fever is distinguished by a gradual onset, with 
abdominal symptoms and a characteristic rash; pneumonia 
appears as a complication late in the disease. 

Prognosis. — The average death rate is about 20 per cent. , but 
with careful treatment amidst favorable surroundings this can 
be greatly diminished. High fever, profound toxemia, the 
involvement of more than one lobe, and heart weakness are 
unfavorable conditions. 

Treatment. — The patient should be placed at absolute rest and 
his diet should consist solely of liquids, especially if the tem- 
perature be high. The surface of the body should be sponged 
frequently. Excessive local pain may be relieved by a hot 
poultice. Hyperpyrexia may require cold sponging or the use 
of the ice pack. Heart weakness demands the use of stim- 
ulants; alcohol, strychnine, or camphor. 

In the hyperemic stage, sthenic cases may be modified by 
the administration of aconite or vcratrum viride ; asthenic 
patients, especially those already feeble and debilitated, derive 



INFECTIOUS DISEASES. 59 

greater benefit from ferritin plios. At any stage of the dis- 
ease marked pleurisy will suggest the use of bryonia. 

With the development of consolidation, the symptoms may 
suggest the use of phosphorus. This remedy is of especial 
value in patients of middle or advanced age, in whom the 
pneumonia occurs secondarily or in association with typhoid 
symptoms. Sulphur is indicated in pneumonias uncompli- 
cated by pleurisy or bronchitis, and occurring at the extremes 
of life. 

In the stage of resolution, cases associated with marked 
bronchitis and diffuse moist rales are benefited by antimon. 
iodid. Purulent infiltration suggests stannum iodid. Tartar 
emetic is demanded by marked pulmonary failure, with edema, 
loud rales, and cyanosis. Antimon. arson, may be used under 
similar conditions. 

The development of a typhoid state will require the admin- 
istration of such remedies as agaricus, arsenic, baptisia y 
bryonia, hyoscyamus, phosphoric acid, and rhus tox. 

ASIATIC CHOLERA. 

Etiology. — The exciting cause is the comma bacillus, which 
gains entrance with food or drink, and is thrown off with the 
intestinal discharges. The disease is endemic in India and 
thence spreads along lines of travel to become epidemic in 
other counties. 

Pathology. — There is no specific lesion. A catarrhal inflam- 
mation of the mucous membrane of the intestinal tract is 
associated with a serous drain which causes the blood to be- 
come thick and dark, while all the tissues become dry and the 
body appears shrivelled. The disease is essentially a poison- 
ing of the system with the toxins of the comma bacilli. 

Symptoms. — The attack begins with diarrhea accompanied 
by prostation and gastric disturbances. In some cases the 
disease is controlled at this early stage and recovery ensues in 
a few days {cholerine'). Otherwise, the diarrhea becomes a 



60 INFECTIOUS DISEASES. 

copious purging. The stools soon lose their fecal character 
and are composed of frothy serum containing flakes of desqua- 
mated intestinal epithelium — the "rice water" stools. The 
passages are usually painless, though griping may occur. At 
this stage severe and persistent vomiting appears; first the 
stomach contents are thrown off, then "rice water;" and 
severe muscular cramps, with retention of urine and the phe- 
nomena of collapse, ensue. The surface of the body becomes 
cold, shrivelled, and covered with clammy perspiration. The 
surface temperature is depressed, although internally it may 
be elevated. The pulse becomes rapid, thready, often imper- 
ceptible. This constitutes the "algid stage" which lasts for 
several hours and often ends in death. Consciousness may be 
retained almost to the end. In favorable cases the vomiting 
and diarrhea gradually cease, collapsic symptoms disappear, 
warmth returns, urine is again secreted, and this stage of re- 
action is followed by convalescence. 

Cholera runs a rapid course, most of the fatal cases termi- 
nating within 24 hours. In patients who recover, convalescence 
may be prolonged over two or three weeks by complications, 
such as nephritis, pneumonia, pleurisy or multiple abscesses. 

Diagnosis. — Doubtful cases of cholera may be diagnosed by 
the recognition of the comma bacillus in stained preparations 
of mucous floccules from the dejecta, by the behavior of cul- 
tures, or by the agglutination test, 

Prognosis. — Guarded. The mortality averages 50 per cent. 

Treatment. — Prophylaxis may be attained by quarantine, 
personal cleanliness, and care in boiling the drinking water 
and cooking the food. 

Infected patients should be put at rest and use of the bed 
pan enforced. All discharges must be disinfected. Withhold 
food until the symptoms are controlled. Cracked ice or iced 
champagne may be given to assuage thirst; and abdominal 
pain may be relieved by hot applications. Hot general baths 
aid in controlling the severe muscular cramps and stimulate 
the circulation. The extreme loss of fluid may be compen- 



INFECTIOUS DISEASES. 61 

sated by the intravenous or hypodermatic use of saline solu- 
tions. 

Of remedies, administer camphor in drop doses on sugar 
during the initial stage. When diarrhea, vomiting, cramps, 
and failing circulation appear, cuprum, cuprum arseu., or 
vcrat. alb., should be given. Later, when reaction is estab- 
lished, baptisia, bryonia, or rJius may be indicated; or the 
suppression of urine and symptoms of nephritis will afford 
indications for the use of cantharis, rJius tox., or terebinth. 

DIPHTHERIA. 

Etiology. — The exciting cause is the Klebs-Loeffler bacillus. 
Secondary infection with pyogenic cocci may occur. The dis- 
ease is endemic in the large towns, occasionally becoming 
epidemic. Childhood amidst unhygienic surroundings favors 
infection. 

Pathology. — The bacilli find lodgment upon the mucous 
membrane of the tonsils, pharynx, larynx, trachea, or nares 
(rarely that of intestines or vagina), and give rise to a fibrin- 
ous exudate with necrosis of the epithelial structures (diph- 
theritic membrane ) which extends to contiguous parts. Me- 
chanical interference with respiration and deglutition ensues; 
and at the same time a violent toxin is thrown into the circu- 
lation and occasions rapid degenerative changes in the viscera. 
The accompanying pyogenic cocci may be absorbed, thus add- 
ing a pyemic factor to the disease. 

Symptoms. — These are local, varying according to the loca- 
tion of the lesion, and general, due to the violent toxemia. 

Local. — More or less local soreness or pain is complained of, 
especially if the lesion be in the throat; and examination dis- 
closes at first a hyperemia of the mucous membrane, soon 
followed by the appearance of an exudate. The latter may 
develop in one spot or in a number of patches which rapidly 
coalesce; it is grayish or yellowish in color, and attempts to 
remove it expose a raw, bleeding surface beneath. Under the 



62 INFECTIOUS DISEASES. 

microscope it is seen to consist of leucocytes, bacteria, and 
-degenerated epithelial cells in a mesh of fibrin. 

As a rule, the disease, if it invades the nasal cavities or the 
larynx, spreads to them from the throat; but it may occur pri- 
marily in either. Nasal diphtheria is usually attended by a 
purulent or bloody discharge and grave constitutional symp- 
toms, and examination reveals the false membrane on the 
nares. Laryngeal diphtheria {membranous croup} is accom- 
panied by hoarseness, croupy cough, and gradually increasing 
dyspnea and cyanosis. False membrane may be expectorated. 

General. — The invasion is usually insidious, the symptoms 
being those of other febrile attacks, i. e. } headache, lassitude, 
and digestive disturbances. The temperature is not high, and 
is often irregular. If the disease is not controlled at the out- 
set, profound systemic poisoning leads to severe nervous 
symptoms (delirium, stupor, coma), or to sudden or gradual 
heart failure. Erythematous or purpuric skin eruptions may 
appear. Albuminuria is frequent, but actual nephritis is rare. 

Complications.— Extension of the membrane to the bronchi 
and lungs occurs in many fatal cases. Hemorrhages may result 
from the ulceration and erosion of mucous surfaces. Paralysis, 
due to a toxic peripheral neuritis, is a common complication 
or sequel: it may involve the nerve supply to the heart, the 
soft palate, the eye muscles, the larynx, or other portions of 
the body. 

Diagnosis. — The discovery of the membrane usually suffices 
for diagnosis. Occasionally swelling of the glands at the 
angle of the jaw, accompanied by grave constitutional symp- 
toms, precedes the appearance of the false membrane in the 
throat. In doubtful cases it is advisable to submit a culture to 
expert examination for the bacillus. 

Follicular tonsillitis may closely resemble diphtheria and 
any doubt requires its treatment as a case of the more serious 
disease. As a rule, however, the exudate of tonsillitis can be 
seen to have orginated in the crypts, it is limited to the tonsil, 
and its removal is easy and reveals uninjured mucous mem- 
brane beneath. 



INFECTIOUS DISEASES. 63 

Scarlatina sometimes presents a pseudo-diphtheria, a 
phlegmonous throat-lesion due to streptococcic infection. The 
sudden onset and typical rash serve to distinguish the disease. 

Prognosis.— Guarded. The former mortality averaged 25%, 
but by the use of antitoxin this has been greatly reduced. Ex- 
tension to nares or larynx and evidences of profound toxemia 
render the outlook more grave. 

Treatment. — Isolation, rest, and nutritious liquid diet. Ad- 
minister at once 1000 to 2000 units of antitoxin, according to 
the age of the patient. Should improvement, evidenced by 
lessening pyrexia and checking of the spread of the mem- 
brane, fail to appear in six hours, repeat the injection; and 
continue to do so at similar intervals until the disease is con- 
trolled. The injections may be made into the buttocks or the 
subscapular spaces. 

Previous to the discovery of the specific antitoxin, much 
good was accomplished by the use of such medicines as apis, 
lachesis, mercur. corros. and cyan., cant haris, rhus tox., and 
the potash salts {kali bich., carb. and c/ilor.). 

Sprays of boric acid or hydrogen dioxide (1-10) may be 
used to cleanse the throat. Laryngeal stenosis may demand 
intubation or tracheotomy for its relief. Profound prostration 
or heart failure requires the administration of alcoholic 
stimulants. 

Post-diphtheritic paralysis is benefited by such remedies as 
gelseminm, cocculus or chloride of gold, together with the use 
of the galvanic current. The anemia of convalescence affords 
an indication for the use of arsenic iodide or the various iron 
combinations. 

ERYSIPELAS. 

(St. Anthony's Fire.) 

Etiology.— The specific cause is the streptococcus pyogenes, 
which gains entrance through some break in the integument. 
Among predisposing causes are the various cachexias, debility, 
wounds, and contact with infected cases. 



64 INFECTIOUS DISEASES. 

Pathology. — This disease is a specific inflammation of the 
skin. It varies from an involvement of the superficial strata 
to an intense phlegmonous change extending to the subcu- 
taneous structures, which are filled with serum, leucocytes, and 
streptococci. 

Symptoms. — Local. — The usual point of invasion for the 
streptococci is about the head, especially the nose, face, or 
ear; but they may find entrance at any part of the body At 
this point on the skin redness and swelling appear, together 
with smarting and burning sensations. The inflammation 
spreads visibly from hour to hour, a well-defined elevated 
margin separating it from the normal skin. Vesiculation and 
suppuration, and even gangrene, may occur in connection with 
the inflammatory process. The disease may involve the 
mucous tracts with serious results. As a rule, the area in- 
volved is limited, the disease being controlled within a week 
or two; but in the so-called "ambulatory" cases the inflam- 
mation may continue to spread until each portion of the body 
surface has been involved in turn. 

General. — Upon invasion, even before local changes have 
become manifest, the patient is seized with a chill, and this is 
followed by irregular, often high fever, pain in the head and ex- 
tremities, and digestive disturbances. At the cessation of the 
local inflammation the temperature drops to the normal. In 
severe cases the toxemia may give rise to profound prostration 
and dangerous cerebral symptoms, while by its dissemination 
the streptococcus may occasion meningitis, endocarditis, peri- 
tonitis, or pneumonia, and in phlegmonous cases septicemia 
or pyemia. 

Diagnosis. — Erysipelas may be differentiated from a simple 
erythema by its pyrexia, marked systemic disturbance, and the 
elevated margin of the spreading inflammatory lesion. Acute 
eczema presents marked itching, redness, and swelling without 
margin, and fever is absent. 

Prognosis. — While recovery is the rule in uncomplicated 
erysipelas, in the case of a debilitated patient the prognosis 
must be guarded. 






INFECTIOUS DISEASES. 65 

Treatment. — Rest. Nutritious food given frequently in small 
quantities; if much fever, liquid diet. Profound prostration 
may demand alcoholics. 

To the local lesion apply cold water or cloths wrung- out in 
ice water. Antiseptics, such as an ointment of icthyol and 
lanolin (20%), or a weak solution of carbolic acid (2%), may 
be applied with benefit, especially in recurrent cases. Suppur- 
ations and abscesses must be treated without delay in accord- 
ance with general surgical principles. 

Of internal remedies, belladonna is suggested by smooth red 
swelling without vesiculation. Sthenic cases may require 
aconite ox veratrum viride. If vesicles appear, rhus tox. y or 
less often anacarditim or croton tig., will be indicated, while 
marked edema will suggest the use of apis mel. Profound 
toxemia with delirium or coma demands such remedies as hy- 
oscyamus, stramonium and lachesis. Suppuration is met by 
the use of hepar, mercury or arsenic, and recurrences suggest 
the need of sulphur. 

SEPTIC FEVERS. 

Etiology. — Septic organisms and their ptomains may enter 
the system: 

1. Through wounds, surgical or traumatic; 

2. Through the uterus, or tubes, following labor or abortion; 

3. Through the mucous membranes, as a result of tonsillitis, 
typhoid, etc., or from the presence in the bowel of foods con- 
taining ptomains {sepsis intestinalis) ; 

\. As a result of suppurative bone disease. 

SAPREMIA. {septic intoxication) is an intoxication produced 
by the saprophytes of putrefaction, the material being con- 
tained within a more or less closed cavity with absorbent walls. 
Notable examples of this are a putrefying placenta or a blood 
clot within a wound or within the abdominal cavity. The in- 
fection is often a mixed one, and at times it is difficult to 
distinguish the condition from septicemia. The effects vary 
5 



66 INFECTIOUS DISEASES. 

in proportion to the amount of necrosed tissue, and the rapidity 
of absorption: it may kill in a few hours ; it may be checked 
by the exhaustion of the pabulum upon which the saprophytes 
depend for their sustenance and growth ; it may be cured 
quickly by their removal ; or the putrefaction may be 
followed by suppuration. 

Symptoms. — At the outset there may be slight pyrexia, with 
malaise, headache, coated tongue, and anorexia. This is 
followed by a chill, high fever, a rapid, soft pulse, vomiting, 
diarrhea, scanty urine, restlessness, delirium, jactitation, and 
cold sweats. Finally the pulse becomes weak, defecation and 
micturition are involuntary, the patient becomes comatose, 
and death ensues. 

Treatment.— Asepsis and antisepsis afford prophylaxis. Should 
the symptoms of sapremia develop, the surgical indications 
are to relieve pressure, and to evacuate and drain the cavity, 
frequently using irrigation. In severe cases the use of purges 
and enemata, together with hypodermatics of strychnine, may 
be necessary. Among the remedies frequently indicated are 
arsenic, car bo veg., and the snake poisons. 

SEPTICEMIA {septic infection) is a toxemia due to the spread 
of pyogenic bacteria throughout the system and a progressive 
intoxication with the products of these bacteria. The living 
bacteria are present in the blood, where they reproduce them- 
selves ; and as a result, e. g., in post mortem or dissecting 
wounds, rapid systemic infection may take place before the 
development of marked local lesions (primary septicemia). 
As a rule the development of septic germs requires a longer 
period than does the process of putrefaction, and therefore 
sapremia occurs earlier than septicemia. 

Symptoms.— A variable period of incubation is followed some- 
times by a chill, always by a rise of temperature, headache, 
anorexia, alimentary disturbances, and a typhoid state. The 
infection spreads by way of the lymphatics, whose course is 
marked by the red line of lymphangitis ; the glands are in- 
flamed (lymphadenitis), and the spleen and bone marrow be- 



INFECTIOUS DISEASES. 67 

come involved. Diarrhea and faint jaundice are common ; 
and various skin eruptions, erythematous or the result of 
thrombosis of the dermal capillaries, may appear. Leucocytosis 
is present. Degeneration of the heart muscle is indicated by 
the rapid and weak pulse ; and endocarditis or pericarditis 
may supervene. The skin becomes cold and clammy, the 
patient is prostrated and indifferent, colliquative diarrhea sets 
in, the urine becomes scanty or suppressed, and finally there 
come delirium, stupor, coma, and death. Local symptoms 
are present at the point of infection : there is edema and red- 
ness of the edge of the wound, with an offensive discharge or 
actual sloughing. The microscope reveals capillaries filled 
with infected thrombi, and the vessel walls and lymph spaces 
are infiltrated with micro-organisms. 

Treatment. — Local. Find the cause: open the wound, evac- 
uate the clot, cut or scrape away the sloughs, cauterize living 
tissue, even amputate if necessary. Hot water or antiseptic 
poultices may be used locally. 

General. Support the patient's strength with nourishing 
food (milk, peptonoids, eggs, fruit) and administer stimulants 
(alcohol, strychnine) if necessary. The leading remedies are 
arsenic, belladonna, carbo veg., and rhus tox. Antistrepto- 
coccic serum may be administered. 

PYEMIA is a toxemia induced by pyogenic organisms, living 
bacteria being transported by the blood current to distant tis- 
sues where they multiply and produce abscesses (multiple or 
metastatic abscesses). It is, in short, septicemia plus an em- 
bolism which spreads infection to distant parts. Pyemia may 
be due to surgical operations or injuries, e. g., compound 
fractures, injuries to veins, etc. It may appear to be "spon- 
taneous" or "idiopathic," usually as the result of osteomyel- 
itis, appendicitis, obscure middle ear disease, etc. 

Symptoms. — The typical manifestations of pyemia require 
ten days or more for their development, but they may be pre- 
ceded by indefinite septic symptoms, or by actual septicemia. 
Following this period of incubation, the patient is seized with 



68 INFECTIOUS DISEASES. 

a chill, which is repeated whenever a fresh suppurative focus 
is set up. The temperature range is septic in type; i. e., fever 
is intermittent and so irregular that it may be necessary to 
take the temperature every two hours in order to trace the 
abrupt changes. Sweats accompany the frequent falls in tem- 
perature. Local symptoms are added to the general signs of 
suppuration, and vary according to the organ attacked; for 
example, if the lungs, there will be pain, dyspnea, cough, and 
expectoration; if the liver, jaundice and symptoms of hepatic 
abscess; if the heart, ulcerative endocaditis, etc. A very 
characteristic condition is suppurative arthritis, especially of 
the sterno-clavicular articulation; it is painless unless com- 
plicated with a metastatic osteomyelitis. The mind is usually 
clear, the patient being restless and hyperesthetic. 
Treatment. — That of septicemia. 



SCAELET FEVER. 

(Scarlatina; Scarlet Rash.) 

Etiology. — The exciting cause, while probably a micro-organ- 
ism, remains undiscovered. The disease is communicated by 
direct contact, by fomites, and by food, the bearer of the con- 
tagium being the desquamated epithelium. Children are par- 
ticularly susceptible. One attack confers immunity as a rule. 

Pathology. — The only characteristic lesion is that of the skin, 
which becomes hyperemic and swollen, the inflammation 
leading to death and desquamation of the epidermis. The 
mucous membrane of the throat is erythematous, and second- 
ary changes occur in the cervical glands, the ear, and the heart, 
kidneys, and other viscera as the result of fever and septic 
conditions. 

Symptoms. — 1. Onset. The invasion is sudden; there may 
be chills or chilliness, or in young children convulsions, and 
sore tliroat, vomiting and high fever develop quickly. The 
face is flushed, the eyes dry and dull, and the tongue is coated 



INFECTIOUS DISEASES. 69 

with a thin white fur through which the papillae stand out in 
distinct red points — the "strawberry tongue." 

2. Fever. The temperature rises rapidly to 103° or more at 
the outset, remains high for three or four days until the erup- 
tion has appeared, and then falls by lysis, reaching the normal 
point within two weeks. 

3. General febrile symptoms. The patient is restless, and 
complains of headache; respiration is rapid, the bowels are 
constipated, and the urine is scanty, high-colored and often 
albuminous. Delirium, coma, and convulsions may ensue; 
the latter, occurring late in the disease, strongly suggest 
the possible presence of uremia. 

4. Throat symptoms. The mucous membrane of the throat 
is red and there is soreness, with swelling of the tonsils and 
fauces, often causing dysphagia. An exudate resembling that 
of follicular tonsillitis or even diphtheria may appear on the 
tonsils. 

5. Eruption. The rash appears on the second day and con- 
sists of discrete, closely packed red points, with reddening of 
the skin between them so that the entire surface appears 
scarlet. It begins about the upper chest and soon covers the 
whole body. It disappears on pressure, as when the finger 
nail is drawn across it, but returns in a few seconds. In ex- 
ceptional cases the eruption may be patchy or may not appear 
on some parts of the body, and in a few malignant cases it 
becomes petechial. It begins to fade at once, and desquama- 
tion follows; the latter varies, according to the severity of the 
case, from fine scales to large flakes. 

Varieties. — 1. Scarlatina simplex, the ordinary type just de- 
scribed. 

2. Scarlatina anginosa, in which throat symptoms are se- 
vere, the false membrane resembling that of diphtheria, and 
local suppuration ensues. 

3. Scarlatina maligna, in which toxemia is so profound 
that death may occur before the usual symptoms have fully 
developed. 



70 



INFECTIOUS DISEASES. 



4. Scarlatina hemorrhagica, in which hematuria, epistaxis, 
and ecchymoses are prominent. 

Complications. — The most common as well as serious compli- 
cation is acute nephritis, which appears in the third or fourth 
week, when desquamation is nearly completed. The patient 
becomes restless, feverish, passes a small quantity of dark 
urine, and dropsy makes its appearance. (See acute paren- 
chymatous nephritis). Among other common complications 
are glandular suppurations, otitis media, arthritis, endocar- 
ditis, and pneumonia. 

Diagnosis. — In mild cases without distinctive eruption, doubt 
may be removed by the discovery of desquamated scales in the 
underclothing or by the evidences of nephritis. 

SCARLET FEVER. MEASLES. DIPHTHERIA. 

Onset. Sudden, with vom- Gradual, with coryza Gradual, 

iting. and photophobia. 



Rash. 


Scarlet color,seen on 


Darker patches, seen 


. None typical. 




upper chest with- 


on face on 4th day. 






in 36 hours. 






Temperature. 


High. 


High, but drops on 
appearance of rash. 


Low. 


Throat. 


Much congested. 


Not involved. 


Dark red early. 


Exudate. 


If present, resem- 
bles follicular 
tonsillitis. 


None. 


Characteristic. 


Cervical glands. 


Usually involved. 


Not involved. 


Involved. 



Prognosis. — Guarded; the mortality varies from 5 to 30 per 
cent, in different epidemics. 

Treatment. — The patient must be placed at rest in an isolated 
room, the diet must be liquid, water may be given freely, and 
tepid sponge baths are advisable. During the early stages, 
aconite is indicated in sthenic cases with great restlessness, 
belladonna in drowsy and dull patients, gelsemium in dull, 
prostated cases, and veratrum viride in cases manifesting 
arterial rather than mental excitement. If the eruption does 
not appear within 36 hours, place the patient in a hot bath 
(100°) for ten minutes, and repeat in 3 or 4 hours if necessary. 

Upon the appearance of the eruption rhus tox. is often indi- 



INFECTIOUS DISEASES. 71 

cated. Marked nervous symptoms, with a tendency to coma 
or convulsions, will require the administration of such reme- 
dies as ailantJuis, camphor, cuprum, hydrocyanic acid or zinc. 
Severe throat symptoms will afford indications for apis, 
arsenic, belladonna, the mercurials, lachesis, or rims. Sup- 
purative conditions require such remedies as arsenic, hepar, 
mercury and sulphur. Aural, renal and other complications 
must receive appropriate treatment. 



MEASLES. 

(Rubeola; Morbilli. ) 

Etiology. — The excitiiig cause is an unknown micro-organism. 
The disease occurs in epidemics, occasionally sporadically, 
and is usually conveyed by personal contact, rarely by fomites. 
The contagium is present in the nasal, bronchial and other 
discharges, as well as in the exfoliated epidermis. 

Pathology. — Measles occasions no apparent change in the 
tissues, the only lesions found post mortem being the result 
of complications, such as pneumonia and nephritis. 

Symptoms. — 1. Catarrhal Symptoms. — At its onset the dis- 
ease resembles an ordinary coryza, with excoriating discharges 
from eyes, nose, and throat, photophobia, and dry cough. 

2. Fever. — The temperature rises moderately at the outset 
(102-104°), but on the second day there is a decided remission 
which lasts until the eruption appears on the fourth day; then 
it rises rapidly, but falls again as soon as the rash is estab- 
lished. 

3. Koplik 's Sign. — On the second or third day minute bluish 
white specks surrounded by a red areola appear on the mucous 
membranes of the cheeks and lips. 

4. The eruption appears on the palate about the third day 
in the form of numerous red points and blotches. On the 
fourth day the rash appears on the skin, first on the face and 
then over the entire body. At first it is red and punctiform, 
but in a few hours the small rounded red spots become slightly 



72 



INFECTIOUS DISEASES. 



elevated, and as they enlarge form patches which are often 
crescentic in form and, as a rule, disappear on pressure. 
At the end of two or three days the rash fades gradually and 
fine desquamation ensues. 

"Black" measles is a malignant type of the disease charac- 
terized by subcutaneous extravasations of blood, hemorrhages 
from the mucous surfaces, and profound prostration which 
often leads to death. 

Complications. — Ophthalmia, otitis, stomatitis, laryngitis, 
broncho-pneumonia, and nephritis. 

Diagnosis. — 

Eruption. 



Measles. 
Rubella. 
Scarlatina. 

Variola. 
Varicella. 

Erysipelas, 



Occurrence. 



4th day. 



Within 48 

hours. 



Within 24 

hours. 



4th day. 

Within 12 to 24 
hours. 

Within 24 

hours. 



Character. 



Small red mac- 
ules, crescen- 
tic borders. 

Round red dis- 
crete mac- 
ules. 

Diffuse, red, 
punctate. 



Umbilicated 

pustules. 

Crops of vesi- 
cles. 

Bright red, pol- 
ished, with 
raised mar- 
gins. 



Duration. 



4 to 5 days. 

3 days. 

7 to 10 days. 

21 to 25 days. 

5 to 8 days. 

4 to 8 days. 



Desquamation, 



Face, thenjBranny. 

body. 



Face and scalp, 
then bodv. 



Slight, branny. 



Neck and Scales. 

Chest, then 

face and 
bodv. 



Face, then 
body. 

Back, chest, 
arms. 

Face. 



Duration oj 
Disease. 



Crusts. 
Crusts. 
Branny. 



2 weeks. 
4 to 7 days. 
2 to 3 weeks. 

4 to 5 weeks. 

2 weeks. 

r to 3 weeks. 



Prognosis. — In healthy children with good surroundings the 
prognosis is generally favorable. Complications may render it 
grave. 

Treatment. — Place the child at rest in a large, dark, well- 
ventilated room, restrict the diet to milk, soups, etc., and 
continue these measures until the temperature has been 



INFECTIOUS DISEASES. 73 

normal for a week. The patient should be bathed daily in 
tepid water, and the eyes and mouth cleansed with a simple 
antiseptic solution, such as boric acid, 10 grains to an ounce 
of distilled water. 

The early febrile symptoms will suggest the use of aconite, 
veratrum viride, or belladonna. The catarrhal symptoms, if 
prominent, will require such medicines as euphrasia, kali 
bichrom. or Pulsatilla. If the bronchial tubes are severely 
attacked, a dry cough will require bryonia, drosera, sticta or 
lacJiesis ; and free secretion will indicate the need of antim. 
tod., arsen. or tartrate. 



RUBELLA. 

(Rotheln; German Measles.) 

Etiology. — The exciting cause of this mild, though highly 
contagious, disease is an unknown micro-organism. It occurs 
in epidemics, rarely sporadically, and generally affects chil- 
dren. 

Symptoms. — Without appreciable prodromes, the patient be- 
comes mildly feverish (100°), and may complain of chilliness 
or headache. On the first or second day an indistinct macular 
eruption appears and develops into pale-red papules, which 
may remain discrete like measles {rtibella morbilliforme) or 
may become small, bright red and diffuse, resembling scarlet 
fever {rubella s car latini forme) . Glandular enlargements can 
be detected about the neck, and the patient complains of sore 
throat. The eruption may spread over the entire body, 
but it fades rapidly and in the course of a week it and all 
other symptoms have disappeared. , 

Prognosis. — Good. Complications are almost unknown. 

Treatment. — Rest, light diet, and such remedies as acouite y 
belladonna, Pulsatilla and rhus. 



74 



INFECTIOUS DISEASES. 



VARIOLA. 

(Smallpox.) 

Etiology. — The disease is highly contagious, the virus being 
thrown off by the lungs and skin, and few of those unprotected 
by vaccination escape infection if exposed freely. The 
poison may remain latent in fomites for years. The specific 
organism has not yet been recognized. 

Pathology. — The essential lesion is an inflammatory cellular 



Temp 



IDay of Disease 



12 3 4 5 



10 11 12 13 14 15 16 17 18 19 



Temp 

c. 



106 
105 
104 
103 
102 
101 
100 
99 
98 



i 




mi 




liii 



liliiill 



41 



40 



39 



38 



37 



Invasion | Papules | Vesicles | Pustules | Crusts | Desquamation. 

Fig. 7. Chart showing the Temperature Curve and Course of the Eruption 
in Small-pox (Salinger-Kalteyer). 

infiltration of the rete miicosiun, accompanied by profound 
toxemia and the consequent degenerative changes in the 
viscera. 

Clinical Course. — -The onset is sudden, a violent chill being 
followed by a rise of temperature to 103° to 104° in the first 
twenty-four hours, with a more gradual but continued rise for 
the next three days. At this time headache and backaclie are 
very severe, and may be accompanied by pains in the limbs, 
nausea, vomiting and photophobia. 



INFECTIOUS DISEASES. 



75 



The eruption appears especially on exposed portions of the 
body about the fourth day. At first it consists of small red 
macules, which rapidly change to papules and give a " shotty 
feel" to the skin. About the sixth day these papules become 
converted into clear vesicles with umbilicated centres. By the 
eighth or ninth day of the disease the vesicle becomes a pus- 
tule and umbilication disappears. At this time the skin 
between the lesions becomes swollen and edematous, and the 
patient's features are hideously unrecognizable. In about 
three days more the pustules begin to dry up and form offen- 
sive smelling crusts which, falling off, leave permanent scars 
or "pock-marks." Frequently the eruption involves not only 
the whole surface of the body but the mucous membranes of 
the respiratory and gastro-intestinal tracts. 

With the appearance of the eruption the temperature falls 
suddenly, but not quite to normal, and the constitutional 
symptoms lessen greatly. When the pustular stage is reached, 
however, a secondary or suppurative fever occurs; the temper- 
ature rises again and the severe symptoms return. As dessica- 
tion occurs the fever falls gradually until finally convalescence 
begins. 

Varieties. — I. Variola vera, which is divided into two forms: 
Variola discreta, in which the lesions are isolated; and variola 
confluens, in which the pustules become confluent. 

II. Variola hemorrhagica (black smallpox), which is divided 
into purpura variolosa, in which blood appears in the papules 
in the first days; and variola hemorrhagica pustulosa, in which 
blood appears in the vesicle or pustule, at times in association 
with hemorrhages from mucous surfaces. 

III. Varioloid, a modified smallpox, mild in its course, 
which attacks those protected by a previous attack or by 
vaccination. 

Complications. — Inflammations of the eye and ear; bronchitis; 
catarrhal pneumonia; abscesses and localized gangrene. 

Diagnosis. — Prior to the appearance of the eruption, diagnosis 
is difficult, although the sudden high fever with intense head- 



76 INFECTIOUS DISEASES. 

ache and backache is significant, and the " shotty feel" be- 
neath the skin is yet more so. Chicken pox presents a similar 
eruption, but the latter appears in successive crops and is 
not accompanied by high fever. 

Prognosis. — The mortality varies with the severity of the 
epidemic and the previous condition of the patient; it is rarely 
below 20 per cent. Confluent and hemorrhagic cases are ex- 
tremely fatal. 

Treatment. — Promptly isolate the patient in a well-aired room, 
and restrict his diet to liquids. The immediate vaccination of 
every individual exposed to infection is imperative. 

Local antiseptic treatment, designed to prevent pitting, 
may be instituted ; it consists in covering the exposed portions 
of the body with cloths soaked in a solution of mercuric 
chloride, 1-10000. When pus forms, evacuate with a fine 
needle and apply carbolized dressings. 

In the stage of invasion the remedies indicated may be 
aconite, belladonna, gelsemium or veratrum viride. In the 
stage of eruption indications are often present for the admin- 
istration of rJius tox., apis mel., baptisia, croton tig., sulphur, 
tartar emetic or thuja. Vaccine virus has been given inter- 
nally with benefit to the patient. Hepar has been employed 
to limit the suppuration. Hemorrhagic cases require such 
remedies as lachesis, crotalus, Jiamamelis, phosphorus, hydro- 
chloric acid and arsenic. 

VACCINATION. 

(Vaccinia.) 

The inoculation of human beings with the virus of cowpox 
was introduced by Jenner in 1798, and to its efficacy in the pre- 
vention of smallpox must be attributed the virtual disappear- 
ance of that frightful pest. 

The method of vaccination is extremely important. Lymph 
taken from a healthy cow and freed of impurities by preserva- 
tion in glycerine, should be used. The spot selected for the 
introduction of the virus is usually over the insertion of the 






INFECTIOUS DISEASES. 77 

deltoid in the left arm, or on the outer aspect of the thigh im- 
mediately above the knee. After careful cleansing, a small 
area of skin is denuded superficially with an ordinary scalpel 
until red serum begins to ooze. The vaccine virus is then 
rubbed in, and the part is exposed to the air until thoroughly 
dry and is afterwards covered with a shield. 

The course of a primary vaccination should be typical. In 
a normal case a papule appears on the second or third day 
and about the fifth day this becomes an umbilicated vesicle 
surrounded by an inflammatory zone. About the eighth day 
the vesicle changes to a pustule, and by the twelfth day a crust 
has formed, which subsequently drops off and leaves a scar. 

Every child should be vaccinated, preferably between the 
second and third months of life, and thereafter every seven 
years. Occasionally hot weather or ill health may justify a 
postponememt. The presence of an epidemic of smallpox 
demands immediate vaccination or re-vaccination without 
regard to circumstances. 

Complications of vaccination, such as ulceration, erysipelas, 
or septicemia, are positive evidence of fault on the part of the 
virus or the vaccinator. Fortunately they are extremely rare. 
Should they occur, the treatment must be conducted on gen- 
eral principles. 

VAEICELLA. 

(Chicken-pox.) 

Etiology. — This is a mild infection, usually occurring in child- 
hood; it is contagious, but the specific cause has not been 
determined. 

Symptoms. — Small red spots appear on the skin and mucous 
membranes and develop rapidly into vesicles, which in a day or 
so dry up into crusts and fall off, leaving no scar. Fresh crops 
of eruption appear on each of the first few days, so that all 
stages are present at one time. Rarely it becomes pustular 
and leaves a scar. The attack is accompanied by febrile 
symptoms and a slight rise of temperature. 



78 INFECTIOUS DISEASES. 

Diagnosis. — The lesion is superficial, rarely umbilicated, and 
lacks the red areola seen in smallpox; it appears in crops and 
involves the surface of the trunk to a greater extent than does 
variola. 

Prognosis. — Absolutely good. Rarely acute nephritis has 
occurred as a sequel to the attack. 

Treatment. — Isolation, rest and light diet, together with the 
administration of rhus tox., mercurius, vaccininum or tartar 
emetic. 



WHOOPING COUGH. 

(Pertussis.) 

Etiology. — The disease is probably due to a specific organism 
whose toxin has a selective action on the centers of the vagus 
and superior laryngeal nerves. As a rule it occurs in children, 
who acquire it by contact, and it is presumed that the virus is 
conveyed in the sputum. 

Pathology. — The only lesions discovered post-mortem are 
those due to complications, such as bronchitis, broncho-pneu- 
monia and pulmonary collapse. 

Symptoms. — 1. Catarrhal stage. The disease begins like an 
ordinary cold, with lachrymation, coryza, dry cough, and 
feverishness. In the course of ten days this merges into the 

2. Paroxysmal stage. The cough becomes violent and 
occurs in paroxysms so prolonged that the patient becomes 
cyanosed and seems in danger of suffocation; then a long, 
crowing inspiration — the "whoop"' — takes place, a quantity of 
glairy mucus is expectorated or vomited up, cyanosis disap- 
pears, and the paroxysm is over. This may be repeated any- 
where from four to fifty or more times in twenty-four hours, 
the severity of the disease being judged by the frequency of 
the attacks. After from three to six weeks the disease passes 
into the 

3. Stage of decline, in which paroxysms become less fre- 
quent and less violent and finally cease altogether. The 



INFECTIOUS DISEASES. 79 

entire course of the disease extends over ten or twelve weeks. 

Complications. — The violent coughing may cause hemorrhagic 
symptoms: such as petechias in various parts of the body, 
epistaxis, hemoptysis, or even sub-dural hemorrhage. Bron- 
chitis, broncho-pneumonia, pulmonary collapse, pleurisy, and 
interstitial emphysema may occur. 

Diagnosis. — By the occurrence of a "whoop." 

Prognosis. — Favorable in the absence of complications. The 
younger the child the greater the danger of the occurrence of 
the latter. 

Treatment. — 1. Prophylaxis. Children, especially the young 
and delicate, must be kept from communication with the 
patient as long as the cough lasts. 

2. General care. Daily exercise in the open air, abundant 
and nutritious food, woolen underclothing, and the avoidance 
of exposure to cold and damp, are essential hygienic details. 

3. Medicines. In the catarrhal stage, aconite, belladonna, 
hyoscyamns, or ipecac may be indicated. Naphthalin may be 
given early and persistently, or with the advent of the parox- 
ysms the symptoms may call for coccus cacti, corallium rubrum y 
cuprum acet., drosera, or mephitis. In severe cases with 
menacing symptoms, spasm of the glottis can be absolutely 
relieved by intubation. 

MUMPS. 

(Epidemic Parotitis.) 

Etiology. — The disease appears in epidemics, is sometimes 
sporadic, attacks children and adolescents by preference, and 
one attack confers immunity. The specific germ is undis- 
covered. 

Pathology. — Inflammatory infiltration of the salivary glands. 

Symptoms. — 1. Pain below and in front of the ear, with dis- 
tress on swallowing. 

2. Enlargement of the salivary glands about the ear, some- 



80 INFECTIOUS DISEASES. 

times accompanied by great swelling of the neck and cheek. 
In two or three days the other side is involved. 

3. Moderate pyrexia (101°) accompanies the invasion. 

4. Involvement of the sexual organs is a peculiar complica- 
tion of mumps; orchitis in males and inflammation of mammae 
or ovaries in women may follow the decline of the parotid 
swelling. 

Diagnosis. — Secondary parotitis, occurring as a complication 
of such acute diseases as typhoid and typhus, is much more 
serious than mumps on account of its liability to suppuration; 
it can easily be distinguished by the history of associated 
disease. 

Enlargements of tlie cervical lymphatic glands, such as 
occur in scrofulous children, are persistent, while the swelling 
due to mumps disappears in about ten days. 

Prognosis. — Favorable, recovery ensuing in the course of a 
week. 

Treatment. — Rest, and the administration of such medicines 
as aconite, belladonna, mercury, rhus, and sulphur. A com- 
plicating orchitis requires support and perhaps strapping of 
the testicles, and Pulsatilla or clematis internally. 

TETANUS. 

(Trismus; Lockjaw.) 

Etiology. — The exciting cause is the tetanus bacillus, a long, 
slender rod with a spore at one end which makes it resemble 
a drum-stick. This organism is widely distributed in the soil, 
in rubbish, etc., but it is anaerobic, and hence man is rarely 
infected. Its mode of entrance is through some wound. 

Pathology. — The virus acts upon the nerve centres of the 
medulla and cord, and these, together with the nerve trunks 
leading from the site of infection, become inflamed. 

Symptoms. — At the onset the patient complains of languor 
and of stiffness of certain muscles, usually those of mastica- 



INFECTIOUS DISEASES. 81 

tion; and in a short time tonic spasm of the latter locks the 
jaws {trismus) . The cervical muscles also become rigid, re- 
tracting the head; the face becomes fixed in a sardonic grin, 
and the muscles of the trunk and of the spinal column become 
rigid, and by their retraction arch the body {opisthotonos, 
plenrostJiotonos, or emprosthoto/ios). At intervals, often from 
very slight external irritation, convulsions occur and entail 
frightful suffering. The temperature is raised (103-106°), the 
pulse is quickened, the body is bathed in perspiration, the 
bowels are constipated, and the urine may be suppressed. 
The mind remains clear to the end. 

Course. — The disease may be acute, violent, and rapidly fatal; 
or it may be sub-acute or chronic, and milder in its mani- 
festations, with a tendency to recovery. 

Diagnosis. — Strychnine-poisoning immediately follows the in- 
gestion of that drug; it begins with gastric disturbance or 
contraction of the extremities, rather than of the muscles of 
mastication; violent convulsions alternate with periods of 
complete relaxation; and examination of the gastric contents 
reveals the presence of strychnia. 

Hydrophobia is distinguished by a history of an animal's 
bite, by laryngeal rather than masticatory spasm, by psychical 
disturbances and by the absence of opisthotonos. 

Tetany is marked by long-continued spasm of the extremi- 
ties, particularly the hands, and lock-jaw occurs late or not at 
all. 

Prognosis. — Grave, the mortality approximating 80 per cent. 

Treatment. — Disinfect and cauterize the wound with nitrate 
of silver; re-open it if necessary. Place the patient at abso- 
lute rest in a room from which light and sound are excluded. 
Feed per rectum. Chloral hydrate, gr. xx-xxx, may be given 
by mouth or rectum to control the spasms; or it may be 
necessary to resort to chloroform inhalations. Strychnine is 
the leading internal remedy; aconite, gelsemiiun, hydrocyanic 
acid, passiflora, and tetanus antitoxin may also be considered. 



6 



82 INFECTIOUS DISEASES. 

ANTHRAX. 

(Malignant Pustule; Splenic Fever; Wool-sorter's Disease.) 

Etiology. — The exciting cause is the anthrax bacillus, an 
organism which especially attacks herbivorous animals; the 
latter derive it from the soil, not from each other. Occasion- 
ally it gains access to the human body through wounds, the bites 
of insects, or with infected food or contaminated air. Those 
associated with cattle or their products, such as hides or hair, 
are necessarily exposed to infection. 

Pathology.— At the point of infection, whether external or 
internal, local inflammatory changes develop rapidly and 
eventuate in gangrene rather than suppuration. The gan- 
grene is due to the mechanical effect produced by the enor- 
mous multiplication of the organisms, which through the blood 
are also enabled to invade every organ. The spleen in partic- 
ular is greatly enlarged, and all the viscera are degenerated. 

Symptoms. — External anthrax. At the point of inoculation, 
usually on an exposed portion of the body, a pimple appears, 
enlarges, and quickly becomes a vesicle filled with blood. 
This bursts, leaving a raw, necrotic surface; and the latter is 
surrounded with a dusky ring of induration, which may be set 
with vesicles. In a few hours severe constitutional symptoms 
set in; there is prostration, fever, and delirium, and death may 
soon occur; but if the slough be thrown off recovery is 
possible. 

Internal anthrax may involve the lungs (wool-sorter's dis- 
ease) or the intestines (intestinal mycosis). Wool-sorters 
disease is characterized by symptoms of bronchitis, with 
dyspnea, pain in the back and legs, and profound prostra- 
tion, which soon ends in death. Intestinal mycosis presents 
the symptoms of acute poisoning, with chill, abdominal pain, 
nausea, vomiting, intense prostration, and death in a few days. 

Diagnosis. — External anthrax must be distinguished from 
ordinary carbuncle. The latter appears oftener upon the back 



INFECTIOUS DISEASES. 83 

of the neck or upon covered portions of the body, pursues a 
less rapid course, is more painful than anthrax, and presents 
multiple openings (''pepper-box lid"). 

Internal anthrax cannot be recognized by its symptoms 
alone. Knowledge of the patient's exposure should lead to a 
search for the bacillus in the blood; it stains readily with 
Loeffler's methylene blue solution. 

Prognosis. — External anthrax, being simply a local infection 
at the outset, can be cured in a majority of cases by early 
cauterization of the lesion, but if unrecognized or untreated, 
the developing toxemia renders it almost certainly fatal. Re- 
covery from internal anthrax is exceptional. 

Treatment. — Prophylaxis should be insured by the cremation 
of the bodies of diseased animals. As soon as the external 
lesion is recognized in man, it should be excised, and its site 
cauterized with the hot iron or acids. 

RABIES. 

(Hydrophobia; Lyssa.) 

Etiology. — The exciting cause, while certainly a micro-organ- 
ism, is unknown. Rabies is a disease of the lower animals, 
especially the carnivora, by whose bite it is transferred to 
man. 

Pathology. — The disease is marked by an inflammatory infil- 
tration in the medulla, especially about the respiratory centre, 
congestion of the cord, and hyperemia of the respiratory 
mucous membrane. 

Symptoms. — 1. Premonitory stage. Following the inocula- 
tion, usually by a dog's bite, there is a prolonged period of 
incubation (2-6 months), and during this period the patient 
may be depressed and irritable, and the wound, after com- 
pletely healing, may show evidences of irritation. 

2. The stage of excitement follows. The patient's face 
betrays intense anxiety, and he becomes so remarkably hyper- 



84 INFECTIOUS DISEASES. 

esthetic that a breath of air or a mere touch may induce a 
violent spasm of the larynx. Through fear of inducing this 
paroxysm he dreads even the sight of water, though he is 
thirsty. His excitement may become maniacal, or repeated 
spasms of the larynx may cause dyspnea, and so lead to the 
emission of curious sounds. During the intervals between the 
paroxysms the patient's mind is perfectly clear. There is 
usually moderate fever, with a rapid pulse and quickened 
respiration. 

3. The paralytic stage supervenes in from one to three days; 
the spasms subside, the patient becomes quiet, general paraly- 
sis gradually develops, and in the course of a few hours he 
becomes unconscious and dies. 

Diagnosis. — Hysteria may develop in those who have been 
bitten by dogs. Such patients try to bark like a dog and to 
bite themselves and others; pulse and respiration are un- 
affected, and by the history and the stigmata the real nature 
of the disease can be determined. 

Prognosis. — When the disease has become established the 
prognosis is hopeless. 

Treatment. — Prophylaxis should be secured by the cauteriza- 
tion of all wounds received in the form of bites, and by pre- 
ventive inoculations with the emulsion made with the cord of 
a diseased animal (Pasteur). During the attack chloral or 
morphine may be given internally, and chloroform inhalations 
may be used in order to lessen the suffering. Belladonna or 
cantharis may be administered on symptomatic grounds. 

GLANDERS. 

(Farcy.) 

Etiology. — The exciting cause is the bacillus mallei, an organ- 
ism which is a little shorter and thicker than the tubercle 
bacillus. The disease is one of horses, but is occasionally 
transferred to man by the inoculation of some small wound 
with the nasal discharge from the animal. In consequence 



INFECTIOUS DISEASES. 



85 



those whose occupation brings them in contact with horses 
are alone liable to the infection. 

Pathology. — At the point of inoculation (usually on the nasal 
mucous membrane or skin) a nodule, composed of round cells, 
develops, and this soon breaks down and forms an ulcer. The 
infection spreads by way of the lymphatics, and ultimately 
the lesions may appear throughout the viscera as well as under 
the skin. 

Symptoms. — At the point of infection a nodular swelling, 
which may vary in size from a pea to a walnut, appears, 
softens, and breaks down to form a spreading ulcer which dis- 
charges fetid pus (farcy) If the nasal cavity be the point in- 
fected, the mucous membrane becomes swollen and studded 
with nodules which subsequently ulcerate; and the destructive 
process may involve the nasal septum, mouth, pharynx, and 
even the lower respiratory tract (glanders). 

In either form of the disease the local symptoms are accom- 
panied by intense prostration, muscular pains, high tem- 
perature, emaciation, and finally the typhoid state and death. 
The disease may be acute, terminating within three weeks, or 
chronic, extending over months. 

Diagnosis. — By the appearance of characteristic nodules, in 
the discharge from which the organism is found. For its de- 
tection, stain a cover glass preparation with warm carbol- 
fuchsin, and decolorize in a 2% solution of nitric acid. 

Prognosis. — In acute cases, unfavorable; in cases of more 
chronic course, about 50% of the patients recover. 

Treatment. — Surgical treatment (cauterization) of the pri- 
mary lesion, with generous nourishment and if necessary stimu- 
lation of the patient. Internally, kali bich., arsenic, or 
graphites may be indicated. 



86 INFECTIOUS DISEASES. 

ACTINOMYCOSIS. 

("Big-jaw;" " Lumpy Jaw," Etc.). 

Etiology. — This disease, which affects both men and cattle, 
is caused by the actinomyces or ray-fungus. The latter gains 
entrance through the mouth, teeth, or pharynx, being intro- 
duced with food or drink; rarely it obtains entry through the 
respiratory tract or skin. 

Pathology — By the growth of the fungus macroscopic yellow 
masses are produced, which vary in size from a millet-seed to 
an orange. The tissues surrounding the tumor become in- 
flamed, and ultimately, as the result of secondary pyogenic 
infection, suppuration occurs. Microscopically the granular 
masses are seen to consist of a closely woven group of conical 
threads with their club-shaped ends outward. 

Symptoms. — Clinically these masses are found in the mouth, 
the respiratory tract, and the alimentary canal. The growth 
of the tumor is slow, causing little pain, but finally it sup- 
purates and discharges a fluid containing characteristic yellow 
granules. If it occurs upon the jaw, the bone becomes en- 
larged and the neck changed in shape. If the lesion is pulmo- 
nary, the symptoms resemble broncho-pneumonia or tuber- 
culosis. The intestinal variety presents the symptoms of 
gastro-enteritis. 

Diagnosis. — Whatever the localization of the lesion, the 
recognition of its nature rests upon the discovery of the fungus 
in the discharges. 

Prognosis. — When the lesion is accessible to surgical inter- 
ference, cure is possible; if not, the patient usually succumbs 
with symptoms of pyemia. 

Treatment. — -Surgical interference if possible; if not, potas- 
sium iodide in large doses. 



INFECTIOUS DISEASES. 87 



TUBERCULOSIS. 

Etiology. — The exciting cause is the tubercle bacillus, a slender 
rod less than half the diameter of a red blood corpuscle in 
length, which gains entrance to the body — 

1. By inhalation, the dust of dried sputum being the ordi- 
nary infective medium. 

2. By the ingestion of infected food, such as the meat or 
milk of tuberculous cattle. 

3. By inoculation, as in the cases of pathologists and others 
working with infected tissues. 

4. By direct parental transmission through the placenta 
(rare). 

Among predisposing causes are: 

a. Tuberculous heredity. 

b. Loss of resisting power, as the result of insanitary living, 
frequent child-bearing and prolonged lactation, occupations 
amid unhealthful surroundings, or exposure to dust-inhalation, 
and certain previous diseases, such as pneumonia, bronchitis, 
diabetes, etc. 

c. Climatic conditions, such as warmth and moisture asso- 
ciated with defective drainage. 

d. Age. No age is exempt, but a large proportion of cases 
occur in early life, the lymphatic glands and bones in children, 
and the lungs in young adults, being especially liable to the 
infection. 

General Pathology of Tuberculosis. —The tubercle bacillus, reach- 
ing the tissue through the inspired air, the lymph, or the 
blood, or with ingested food, produces local irritation at the 
point of its lodgment; and the result is: 

1. The formation of a small grayish granular body, per- 
haps the size of a millet-seed — a tubercle. The steps in its 
formation are as follows: 

(a) Proliferation of the fixed cells of the tissue upon which 



00 INFECTIOUS DISEASES. 

the bacillus has lodged, the new cells being of large size and 
containing a single oval nucleus — the so-called epitheliod cells. 

(b) The formation of a wall of leucocytes around this group 
of new cells. 

(c) The appearance in the midst of the new structure of a 
few very large cells, consisting of coarsely granular protoplasm 
with many nuclei — giant cells. 

(d) Degeneration in the centre of this nodule, which is cut 
off from the blood supply and poisoned with bacterial toxins; 
and this necrotic process soon transforms the central portion 
into a yellowish, cheesy mass. 

Histologically, the tubercle appears to consist of an outer 
layer of small round cells (leucocytes), a middle zone of epithe- 
loid and a few giant cells, and a caseous centre. A fine fibril- 
lary reticulum appears at the margin, the fibrils lying between 
the epitheloid cells; and the tubercle bacillus is present in and 
between the cells in large numbers. A tubercle may coalesce 
with neighboring nodules either before or after it undergoes 
caseation. 

2. Diffuse inflammation of tlie tissues about the tubercle, 
which may become obscured by the rapid filling of the tissues 
with cell-products and inflammatory exudate. The latter 
quickly becomes caseous, and results in a diffuse cheesy infiltra- 
tion, as seen, e. g. y in brain, kidneys, testicles, etc. 

The caseous mass thus formed may undergo: 

(1) Softening. Septic organisms, especially streptococci, 
may gain entrance to the nodule, setting up suppuration; and 
ultimately the pus may be discharged, leaving behind a cavity 
with ulcerating walls. Or, 

(2) Fibrosis. An overgrowth of connective tissue may 
spring up around the nodule, completely encapsulating it; 
and as a result the caseous mass may remain unchanged for 
years, or by deposit of lime salts it may become calcified. 
Tubercular lesions never undergo resolution. 



INFECTIOUS DISEASES. 



89 



ACUTE TUBERCULOSIS. 

(Acute Miliary or General Tuberculosis.) 

Etiology. — By the breaking down of a caseous focus in some 
part of the body — most frequently in lung or lymphatic gland — 
tubercle bacilli are thrown into the blood current and dis- 
tributed throughout the body. Tuberculous lesions are thus 
produced in many organs. Clinically, three distinct forms are 
recognizable, one presenting symptoms of general infection 
without distinct localization, a second presenting predominant 



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Fig. 8. — Chart showing the Irregular Continued Fever of Miliary Tuber- 
culosis. 

pulmonary symptoms, and a third of cerebro-spinal type. 

Symptoms. — I. Typhoid Form. After some days or weeks of 
ill-defined prodromes, there appear — 

1. General Febrile Symptoms. — Headache, mental dulness 
and ultimately delirium and coma occur. The tongue becomes 
dry and brown, there is rapid loss of flesh and strength, and 
sometimes diarrhea or intestinal hemorrhage is associated. 
The occurrence of excessive sweating accompanied by suda- 
mina, and the presence of herpes may serve to exclude typhoid 
fever. 



90 INFECTIOUS DISEASES. 

2. Symptoms due to certain localizations may occur, e. g. y 
cough, usually dry, with hurried respiration, dyspnea and 
cyanosis; pleural friction; pericardial friction; tubercles in the 
choroid coat of the eye. 

3. Pyrexia.— The temperature is high (103°-107°), but 
irregularly and markedly intermittent; occasionally there are 
characteristic "inversions" in which the maximum rise occurs 
in the morning instead of the evening. Pulse and respiration 
are rapid. 

Diagnosis. — Acute miliary tuberculosis. Typhoid fever. 
Epistaxis rare. Epistaxis common. 

Rash unusual. Characteristic rose-spots on 

abdomen. 
Respiration hurried, dyspnea, Respiration regular. 

cyanosis. 
Rales moist, subcrepitant. Rales dry, sonorous, sibilant* 

Temperature irregular, may Temperature shows regular 

be intermittent or inverted. diurnal remission. 
Tubercles may be found on None. 

choroid. 
No Widal reaction. Widal reaction present. 

Prognosis. — Invariably fatal. Toward its termination the dis- 
ease may assume the pulmonary or meningeal type. 

II. Pulmonary form (miliary tuberculosis of the lungs). 
Gradually, sometimes suddenly, the patient develops: 

1. General Febrile Symptoms. — At first there is headache, 
malaise, and loss of appetite; delirium and coma may come 
later. An initial chill is rare. 

2. Pulmonary Symptoms. — These vary. Hemoptysis may 
occur at the outset if there is an old tubercular lesion in the 
lung. Cough is usually present, but is not always severe. 
Expectoration may be absent; if present it is mucoid and may 
be blood-stained. Pleuritic pain is sometimes noted. Dyspnea 
begins early, and as the disease advances the respirations may 
become very rapid (50-80 per minute). Cyanosis appears 
when considerable lung structure is involved and increases to 
the end. 

3. Pyrexia may be slight if debility is extreme; but, as a 



INFECTIOUS DISEASES. 



91 



rule, the pulmonary form is characterized by continuous fever 
(101°-104°) with slight morning remissions. Less often it is 
of the inverse type, attaining its maximum in the morning in- 
stead of the evening. 

The pulse is rapid and feeble, the spleen enlarged, albumi- 
nuria is common, and the typhoid state may develop. 

Diagnosis. — The physical signs are not distinctive, being those 
of broncho-pneumonia. In doubtful cases search should be 
made for old tubercular foci, for tubercles in the choroid, and 
for bacilli in the sputum. The onset of the symptoms of tuber- 
cular meningitis will also confirm the diagnosis. 




Fig. 9.— Chart showing the "Inverted" type of Fever in Miliary 
Tuberculosis. 

III. Meningeal form (tubercular meningitis; basilar men- 
ingitis; acute hydrocephalus). In this form there is a deposi- 
tion of tubercles along the vessels of the pia mater at the base 
of the brain, with an exudation of lymph which renders the 
membranes thick and opaque. For some weeks the patient, 
usually a child, appears indefinitely ill; then he develops— 

1. Intense headache and delirium, with hy peresthesia of the 
special senses. The pain may be excruciating, causing the 
patient to utter penetrating screams (hydrocephalic cry). 
The pupils may be contracted. 



92 INFECTIOUS DISEASES. 

2. Vomiting of cerebral type, without nausea and without 
great effort. 

3. Convulsions, paralysis, and coma. According to the 
localization of the lesion, twitchings of various groups of mus- 
cles may occur, to be followed later by paralysis. Thus there 
may be produced strabismus, ptosis, or paralysis of face or 
limbs. General convulsions may occur. 

4. Respiration becomes slow, irregular and sighing as the 
disease progresses. 

5. Pyrexia develops slowly and is rarely high (102°-103°). 
The pulse is either slow or but moderately accelerated. The 
typhoid state may develop. 

Prognosis. — Unfavorable, the disease usually terminating 
fatally within four weeks. 

Treatment. — In a disease so hopeless, whichever form it may 
assume, little else can be done than maintain the strength 
of the patient by means of rest and nutritious food. Among 
remedies symptomatically suitable are arsenic, the calcareas, 
cinchona, ferritin, hyoscyamus, iodine, phosphorus, rJius tox., 
stramonium, and sulphur. In the meningeal cases apis, bella- 
donna, bryonia, and Jielleborus are also recommended. A few 
cures have been reported as following the repeated applica- 
tion of iodoform ointment to the shaved head. 



TUBERCULOSIS OF THE LYMPHATIC GLANDS. 

(Scrofula; Tuberculous Lymphadenitis.) 

Involvement of the lymphatic glands, especially the cervical, 
bronchial, and mesenteric, is common; they become swollen, 
and in many cases suppurate and finally rupture. 

Cervical lymphadenitis is obvious on inspection or palpation 
of the neck; it is necessary, however, to exclude Hodgkins' 
disease, leucocythemia, and sarcoma. 

Bronchial lymphadenitis may be unaccompanied by symptoms, 
or on the other hand the enlargement may be so great as to 



INFECTIOUS DISEASES. 93 

suggest mediastinal tumor. Symptoms ma} T arise from pres- 
sure upon the pneumogastric or recurrent laryngeal nerves 
(spasmodic cough, dyspnea, hoarseness, spasm or paralysis of 
laryngeal muscles, acceleration or slowing of the heart) or 
from rupture of a softened gland into a bronchus (cough with 
expectoration of pus, blood and bacilli). 

Mesenteric lymphadenitis (tabes mesenterica) may be accom- 
panied by symptoms of associated peritonitis, diarrhea, fever, 
painful and swollen abdomen, and evidences of peritoneal 
effusion. Detection of the nodules, by careful palpation, will 
establish the diagnosis. 

PULMONARY TUBERCULOSIS. 

(Phthisis Pulmonalis; Consumption of the L,ungs.) 

Pathology. — Deposit of the tubercle bacillus in the lungs is 
followed by the formation of — 

1. Tubercles. 

2. Diffuse lesions, including — 

(a) True pneumonic inflammation of the broncho-pneu- 
monic type. 

(b) Proliferation of the connective tissue. 

(c) Inflammation and adhesion of the pleura over the 
affected lung area. 

The areas involved may undergo caseation, destruction, 
and excavation, or they may undergo fibrosis or calcification. 

Varieties. — The forms of pulmonary tuberculosis differ from 
each other simply in the predominance of caseation and 
softening or of fibrosis in the lesion; they are as follows: • 

I. Miliary tuberculosis of the lungs. This variety is marked 
by a rapid formation of miliary tubercles throughout the lungs. 
It may be simply a terminal event in chronic tuberculosis, it 
may follow the break-down of an old encapsulated lesion, or 
it may be primary. It is often associated with the formation 
of miliary tubercles in many other organs, to which the bacilli 



94 INFECTIOUS DISEASES. 

have been conveyed by the blood. (See General Tuberculosis, 
page 89). 

II. Caseous tuberculosis of the lungs (acute pneumonic 
phthisis, florid phthisis, galloping consumption) occurs in per- 
sons whose resistance is so weak that nearly all the lung 
structure in one area after another is involved in the tuber- 
cular process, undergoing rapid caseation and softening. This 
variety may occur in a lobar form, in which there is a massive 
consolidation, a lobe or even an entire lung becoming caseous; 
or, more often, a disseminated form, in which the process be- 
gins in the bronchioles of one or both lnngs, quickly spreads 
to the alveoli, and is distinctly broncho-pneumonic in type. 

III. Fibroid tuberculosis of the lungs represents an extreme 
opposite to the variety just described. The miliary tubercles 
undergo fibrosis before either caseation or softening can occur, 
appearing in the lung as: 

(a) Isolated granulations, indurated and deeply pigmented; 

(b) Groups of such granulations; 

(c) Rounded or irregular areas of induration surrounded by 
fibrous granulations. 

IV. Fibro-caseous tuberculosis of the lungs (chronic, ulcer- 
ative tuberculosis), the common form of the disease, stands 
midway between the purely caseous and the fibroid forms. 
Areas of caseation are formed and often undergo softening and 
excavation, but inflammatory changes at the margin of the 
lesion lead to the production of a fibrous wall which checks 
the advance of the disease for a time. At intervals fresh areas 
are attacked by the infection and occasion active symptoms; 
then the process becomes checked again, and another period 
of apparent latency occurs. In this way the disease may ex- 
tend over months and years. 



INFECTIOUS DISEASES. 



95 



CASEOUS TUBERCULOSIS OF THE LUNGS. 

(Acute Pneumonic Phthisis; Florid Phthisis; Galloping Consumption. ) 

Symptoms. — 1. Onset. As a rule the initial symptoms and 
physical signs are those of any pneumonic process, the onset 
being- attended with fever and cough. Sometimes there is an 
initial chill, and occasionally hemoptysis is the first symptom. 

2. Hectic symptoms. In a short time the fever assumes the 
hectic type, with high temperature, flushed cheeks, hot skin, 



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Tuberculosis. 

night sweats, chills, and rapid emaciation. 

3. The expectoration, at first mucoid and perhaps blood- 
stained, becomes purulent and contains tubercle bacilli. 

4. Pyrexia. The temperature at first is high (101-104°) 
with marked remissions; later, with softening and excavation 
in progress and vitality failing, it may become intermittent, 
with an evening rise to 102° or more, and a morning fall to 
97° or below. 

Physical Signs. — In the broncJio-pneumonic variety the signs 
are those of infiltration, viz., lessened resonance, harsh breath- 



96 INFECTIOUS DISEASES. 

ing, and crepitation, usually at the apices; and these may 
merge into the signs of consolidation, including dulness, bron- 
chial breathing, and bronchophony. In the lobar form the 
symptoms are those typical of pneumonia, viz., percussion- 
dulness, crepitation, and tubular breathing over an extensive 
area. In either form signs of excavation may be detected 
later. 

Diagnosis. — Even though the nature of the infection be un- 
suspected at the outset, the absence of a crisis at the end of a 
week or so, and the rapid pulse, sweating, and unusual emaci- 
ation, will suggest examination of the sputum ; and discovery 
of the tubercle bacilli, often in association with fibres of con- 
nective tissue, will reveal the nature of the process. 

Prognosis. — The disease is rapidly fatal, death occurring 
within periods ranging from two weeks to four months. 

Treatment. — Complete rest, hypernutrition with liquid food, 
stimulants, and hydrotherapy are indicated. The persistent 
use of cold water, applying compresses to abdomen and trunk, 
may prove advantageous. The medicines are those recom- 
mended for the treatment of chronic tuberculosis. 

FIBROID TUBERCULOSIS OF THE LUNGS. 

Symptoms. — The onset is very gradual and marked by few 
symptoms, and the lesion may undergo permanent arrest 
without its existence ever having been suspected. Its presence 
may be indicated, however, by 

1. Hemoptysis, which may be profuse and recurrent, with- 
out evidence of advance of the lesion. 

2. Cough, which is rarely severe and is accompanied by 
little or no expectoration. 

3. Temperature. — There is a more or less complete absence 
of evening pyrexia, with a tendency to subnormal temperature 
in the morning. 

Physical Signs. — 1. Retraction of the supra- and infra-clavic- 
ular regions of one side, with impaired expansion. 



INFECTIOUS DISEASES. 



97 



2. Impaired resonance, unless the latter be masked by 
emphysema. 

3. Breath sounds iveak, expiration prolonged, and fine 
crackling rales. 

Diagnosis. — By physical signs. The latter may, however, be 
masked by emphysema, and in that case doubt can be re- 
moved only by discovery of the tubercle bacilli in the sputum. 

Prognosis. — Fibroid tuberculosis tends to a prolonged course, 
if not complete arrest. 

Treatment. — That of the ordinary chronic form. 




Fig. ii. — Chart showiug the Subnormal Temperature of Fibroid 
Tuberculosis. 



CHRONIC PULMONARY TUBERCULOSIS. 

( Fibro-Caseous or Ulcerative Tuberculosis.) 

Symptoms. — 1. The mode of onset varies greatly; frequently 
it is 

(a) Insidious, the patient simply noting a gradual loss of 
strength with slight cough, little expectoration, anemia, and 
emaciation. Loss of appetite, dyspepsia, and vomiting after 
eating are common; and night sweats and dyspnea may be 
noticed. 



98 



INFECTIOUS DISEASES. 



(b) Hemoptysis may be the first indication of disease. It 
may be followed immediately by the usual symptoms of the 
disease, or the latter may be delayed for some time. 

(r) Pleurisy, either dry or with effusion, often precedes the 
development of the lung lesion. 

(d) Bronchitis, recurring in acute attacks for several years, 
particularly each winter, may finally be followed by evidences 
of tuberculosis. 

(e) Laryngitis, though usually secondary, may occur before 
the lung infection. The patient complains of irritation in the 
larynx, cough, hoarseness and mucoid expectoration. 




Fig. 12.— Chart showing the Temperature in a Quiescent Case of Chronic 
(fibro-caseous) Tuberculosis. 

2. Cough begins early in the course of the disease. At first 
it is dry and hacking; later it is accompanied by expectoration 
and may occasion vomiting and dyspnea. 

3. Expectoration. In the earlier stages the sputum consists 
of mucus, sometimes rendered watery by admixture with 
saliva. When softening occurs the sputum becomes purulent, 
yellow or green in color, and often blood-stained. 

4. Chest pain is common; it may be due to pleurisy, inter- 
costal neuralgia or myalgia. 

5. Pyrexia may vary in its type, according to the activity 



INFECTIOUS DISEASES. 99 

of the disease, and fever may be absent during long periods in 
which the disease is latent. During advance of the purely 
tubercular lesion the evening rise varies from 99° to 100.5°; 
but with secondary infection and softening the evening tem- 
perature is apt to rise much higher, with or without marked 
remissions to indicate its septic character. The pulse is rapid 
and weak throughout the disease. 

6. Emaciation and anemia are generally coincident with the 
progress of the lesion; a gain in weight is therefore suggestive 
of arrest of the process. The anemia is of symptomatic type 
and leucocytosis is absent as a rule, although it may be ob- 
served when suppuration is in progress. 

7. Gastro-intestinal symptoms are frequently prominent. 
The tongue may be coated, appetite lost, and thirst and other 
symptoms of gastric catarrh present. Vomiting may be the 
result of gastritis, but in many cases it simply follows severe 
coughing paroxysms. Diarrhea may result from dietetic errors, 
but when it occurs late in the disease it generally indicates 
intestinal ulceration. 

Physical Signs. — During the stage of infiltration, before any 
extensive consolidation has developed, the more important 
physical signs, generally, but not always, heard at one apex, 
are: 

1. Feebleness of the respiratory sounds, with or without cog- 
wheel breathing. 

2. Prolonged and high-pitched expiration (broncho-vesicu- 
lar breathing) often associated with localized dry rales. 

When considerable solidification has occurred, the signs in- 
clude, in addition to more marked broncho-vesicular breath- 
ing, 

3. Depressed surface, impaired movement during respiration 
and evident loss of flesh, generally. 

4. Percussion dulness over the diseased area. 

5. Increased tactile and vocal fremitus ; increased intensity 
of the whispered voice is especially significant. 

Lor v. 



100 INFECTIOUS DISEASES. 

When softening begins in the consolidated area — 

6. The rales become larger, more numerous, and moist, 
(Moist rales may also be due to the presence of fluid blood; 
this must be excluded.) 

When the process of softening and discharge has produced 
a cavity of large size, it may be recognized by — 

7. Cracked-pot resonance on percussion. 

8. Amphoric or cavernous breathing. 

9. Coarse, gurgling rales. 

Confirmatory evidence of the existence of a cavity may be 
found in other signs, such as a tympanitic percussion note with 
greatly increased vocal resonance (pectoriloquy); Wintrich's 
change of percussion note, the latter becoming higher when 
the mouth is open; and Gerhardt's change of sound, the 
tympanitic note becoming deeper when the patient sits up. 

It must be remembered that all stages of the disease and 
consequently all the above physical signs may be present in 
one lung at the same time. 

Prognosis. — While a majority of these patients finally suc- 
cumb to the pulmonary disease, in all but the advanced stages 
arrest of the lesion and comparative health for years is possi- 
ble. In any given case a prognosis must be based upon con- 
sideration of the following factors: 

1. The constitution and family history of the patient. 

2. The stage of the disease. Arrest is more common in the 
stage of infiltration. 

3. The character of the general symptoms and their rate of 
progress. A poor appetite, digestive disturbances, and evi- 
dent nutritional failure render the outlook dark. Continued 
pyrexia, or the inverted type, are unfavorable, indicating the 
onset of miliary tuberculosis. 

4. The presence of complications, such as laryngeal tuber- 
culosis, diarrhea, albuminuria, or peritonitis, is of unfavorable 
import. 

Diagnosis. — In advanced cases the diagnosis is rarely difficult, 



INFECTIOUS DISEASES. 101 

but in the earlier stages it is often impossible to decide as to 
the nature of the case by symptoms and signs alone. At any 
period of the disease doubt is ended by the discovery of the 
tubercle bacillus in the sputum. For this repeated examina- 
tions may be necessary, and it is essential that the expectora- 
tion so examined shall have come from deep in the chest; 
for this purpose that first raised in the morning is best. Select 
from a thin layer of sputum one of the small caseous particles, 
transfer it by means of a platinum loop to a cover-slip, press 
down upon it a second cover-glass, and separate the two by 
sliding them apart. Allow the cover-glasses to dry in the air, 
and fix the spread by holding each cover-slip, face upward, 
between the ringers and passing it through an alcohol flame. 
Then holding a cover-glass, still face upwards, with a pair of 
forceps, cover the surface with the Ziehl-Nielsen solution of 
carbol-fuchsin (fuchsin, 1 gm. ; carbolic acid crystals, 5 gms. ; 
alcohol, lOc.c. ; distilled water, 100 c.c. ), and pass it slowly 
over the flame until steam arises. Do this seven times, with- 
out allowing the fluid to actually boil. Then rinse it in clear 
water, and counter-stain in Gabbet's solution of methylene 
blue (methylene blue, 1 gm. ; sulphuric acid, 25% solution, 
100 c.c.) for a minute or two. Examine the mounted slip 
under a iV-inch oil immersion objective, and the tubercle 
bacilli will appear as small red rods, pus corpuscles and other 
organisms being stained blue. 
Treatment. — This must include: 

1. Prophylaxis. — Prevent infection by destroying the sputum 
before it becomes dry, and disinfect all other discharges. 
Caution the patient against swallowing the sputum, lest other 
organs become infected. Do not allow a tuberculous mother 
to nurse her children. Let the patient occupy a separate 
room, if possible, and see that the latter is well aired and 
occasionally disinfected. 

2. General Hygiene. — The patient must be clad from head to 
foot in warm but light clothing, wool being preferable to silk. 
He should have a tepid or cold sponge bath on arising in the 
morning, followed by forcible dry friction. Douching and 



102 INFECTIOUS DISEASES. 

massage of the chest wall are often advisable. The patient 
should rest for half an hour or more after each meal, for a 
longer period at mid-day if possible, and in case there is per- 
sistent fever (above 100°) rest in bed must be absolute. The 
amount of exercise must be graduated according to the 
patient's strength and the stage of the disease. Special 
abdominal and respiratory exercises are advisable in the early 
stages. 

3. Climatic Treatment. — The ideal climate for the con- 
sumptive must have an atmosphere free from gases, dust, and 
micro-organisms; it must be dry, and a high altitude is desir- 
able because of its stimulating effect on respiration. On the 
other hand, high altitudes do not agree with weak, debilitated 
patients, especially neurotics, nor with those subject to fre- 
quent or severe hemorrhages. On this account, when the 
patient is sent away from home great care must be exercised 
in selecting his resort. As a rule, a suitable place can be found 
on the great plains bordering the Rocky Mountains, in Colorado, 
New Mexico or Arizona. It is essential that good food be obtain- 
able. Climatic treatment can be carried on at home in many 
cases, the patient spending almost the entire period of day- 
light, summer and winter, at rest in the open air. A reclining 
chair, with suitable protection from the wind, and wraps suited 
to the temperature, render this possible. At night he sleeps 
in a room with open windows, coverings protecting him from 
cold and screens from draught. This method, combined with 
forced feeding, is the foundation of the sanatorium treatment; 
and can also be used with fair success in the patient's home. 

4. Dietetic Treatment. — The patient should eat three full 
meals per day, drinking little and avoiding too much food at 
one time. The diet must be nitrogenous, consisting of meat, 
milk, oysters, fish and eggs. In addition he should take, at 
an interval of half an hour or so after each meal, a luncheon 
consisting of raw eggs, broken into a cup, seasoned with salt 
and pepper, and swallowed without stirring. In this way from 
6 to 12 or more eggs can be taken daily. Pure water may be 
imbibed freely between meals. 



INFECTIOUS DISEASES. 103 

5. General Medicinal Treatment. — Of the many remedies, 
those have proven most useful whose influence is upon nu- 
trition, as, for example, creosote, guaiacol, the hypophosphites, 
and strychnine. The iodine compounds are extremely valuable: 
particularly arsenic iodide in strumous individuals with weak 
hearts and a tendency to diarrhea, and antimony iodide and 
stannum iodide in cases with free muco-purulent expectoration, 
the result of suppuration and excavation. Symptomatic indi- 
cations may be found for many other remedies*. 

6. Symptomatic Treatment. — Fever requires no special 
treatment unless the temperature rise above 100°; in the latter 
case, the patient should be put to bed and given such remedies 
as baptisia, ferrum pJios., quinine ars., or silica. Sponging 
with cold water, or even the wet pack, may prove advan- 
tageous. 

Sweating requires the administration of such medicines as 
agar id n, camphoric acid, ferrum ars., phosphoric acid, picro- 
toxin, pilocarpine, or silica. The patient may be benefited 
by sponging with a saturated solution of alum or some other 
astringent. 

Cough, when essential to the removal of secretion from the 
bronchial tubes, must not be interfered with. In many cases, 
however, the cough is simply the result of irritation at some 
point in the respiratory tract, and its cause, e. g. , nasopharyn- 
geal catarrh, should receive appropriate local treatment. 
Inquiry into the habits of the patient may reveal the fact that 
his evenings are spent in an ill-ventilated room, or that he 
goes from a warm room to a cold bed, and a troublesome 
night cough results. Discovery and removal of such causes 
control the symptom. Rarely is it advisable to resort to an 
opiate; in that case, give codeine, gr. \, or heroin, gr. -jt or rV- 

When expectoration is at all free, antiseptic inhalations are 
valuable. Of a mixture of equal parts of beechwood creosote, 
chloroform and alcohol, place 20 drops on the sponge of a 
Goodno or Yeo respirator, and inhale for 20 minutes; renew 
the solution at these intervals until an hour has been con- 



104 INFECTIOUS DISEASES. 

sumed, and repeat the inhalations, one hour at a time, three 
times a day. Eucalyptus, guaiacol, or terebene can be substi- 
tuted for the creosote. 

Hemoptysis, if profuse, requires that the patient be placed 
at rest in a cool room in a semi-recumbent position. He may 
be given bits of ice to suck, and internally such remedies as 
aconite, geranium, hamamelis, Hydrastis, and hydrastinine 
hydrochlorate. Dangerous hemorrhage, uncontrolled by these 
measures, may require the use of atropin or morphine hypo- 
dermatically. 

Chest pain is usually controlled by quiet and the use of such 
remedies as aconite, actea, bryonia, sciilitin, or kali carb. 
Bathing, massage, friction and counter-irritation may prove 
useful. 

Gastro-intestinal symptoms are of unfavorable import. A 
liquid diet, consisting largely of milk or koumiss, should be 
directed until the symptoms abate, and the return to solid 
food must be gradual. Arsenic, cinchona, copper arsenite, 
ferrum phos., and ferritin ars. are among the important 
medicines. 

SYPHILIS. 

(Pox; Lues Venerea.) 

Etiology. — The specific organism has not yet been discovered. 
Infection may be: 

1. Hereditary. 

(a) From the father, if the latter's infection has occurred 
within three or four years. 

" (b) From the mother, if the latter be in the active stages of 
the disease; if the disease has been acquired some months 
previous to the conception, the child usually escapes. More- 
over, the mother may be infected through the placental circu- 
lation, but a syphilitic child cannot infect its mother after 
birth (Colles' law). 

2. Acquired. 



INFECTIOUS DISEASES. 105 

(a) By inoculation during sexual intercourse. 

(b) By "extra-genital" inoculation, as by infected instru- 
ments, cups, pipes, kissing, etc. 



ACQUIRED SYPHILIS. 

Stages of the Disease. — Three periods are recognized, viz. : 

1. A primary stage, extending from the time of infection to 
the outbreak of constitutional symptoms (8-10 weeks), which 
is divisable into — 

(a) An incubation period of from fourteen to twenty-days, 
which ends with the appearance of the primary sore. 

(b) A seond incubation period extending from the .time of 
appearance of the chancre to the development of constitutional 
symptoms. 

2. A secondary stage, lasting from one to three years and 
marked by skin manifestations. 

3. A tertiary stage, of indefinite duration, marked by in- 
flammatory and destructive lesions (gicmmata) which may 
attack any tissue of the body. 

Pathology. — At least five lesions are characteristic of syphilis, 
viz. : 

1. The initial lesion, the chancre, which occurs at the point 
of inoculation and consists of a vesicle or papule, which be- 
coming softened at its centre, forms an ulcer with a hard, 
gristly base. 

2. The lymphatic glands adjacent to the primary lesion, and 
often those of the entire body, become enlarged. Suppura- 
tion occurs, however, only when there is a mixed infection. 

3. Mucous patclies {moist papules) occur in the secondary 
stage and consist of inflammatory infiltrations of mucous mem- 
branes or of the moist portions of the skin, e. g., the gluteal 
folds. By hypertrophy they may form venereal warts, especi- 
ally about the vulva and anus. 



106 INFECTIOUS DISEASES. 

4. The cutaneous sypliilides may be macular, papular, pus- 
tular, or squamous; their color is apt to be "coppery," they 
excite neither pain nor itching, as a rule, and their distribu- 
tion is usually symmetrical. 

5. The tertiary lesions consist of circumscribed inflamma- 
tory products {gumma) of varying size which tend to disinte- 
grate, forming ulcers, or to become enveloped in granulations 
and connective tissue, the subsequent contraction of which 
forms fibroid indurations. These lesions may appear in con- 
nective tissue, bones, skin, muscles, the visceral organs, etc. 

Symptoms. — Primary stage. Following infection, from 
fourteen to twenty-one days pass without symptoms. Then 
at the site of inoculation a single chancre appears and persists 
for several weeks. When its edges are grasped between the 
fingers its peculiar induration {"parchment induration") may 
be easily recognized, although the latter is not invariably 
present. Enlargement of the lymphatic glands all over the 
body occurs in the course of the next two weeks, those nearest 
the site of inoculation being affected first. 

Secondary stage. In the course of six or more weeks the 
patient develops sore throat, due to hyperemia of the fauces, 
shallow ulcers on the tonsils, or mucous patches; laryngeal 
ulceration may also occur. Associated with these lesions 
there is usually irregular fever, languor, headache, bone- 
pains, and anemia {syphilitic cachexia). Various sypliilides 
now appear; the most common is macular, a diffuse roseola 
coming out over the trunk; papular, pustular, and tubercular 
lesions are apt to appear a little later. At the same time 
falling out of the hair may be noted, and iritis, choroiditis, 
or retinitis is not uncommon. 

Tertiary stage. A period of freedom from symptoms and 
apparent good health usually follows the secondary manifesta- 
tions, and in many patients this is permanent. In less fortu- 
nate cases, however, at the end of a year or more deep-seated 
sypliilides, gummatous nodules, and fibroid indurations develop. 
On the surface the syphilitic rupia, in which laminated crusts 



INFECTIOUS DISEASES. 107 

cover a deep pustule, is common. Gummata may develop in 
the skin or subcutaneous tissues, the bones or cartilages, or 
the viscera, and undergo ulceration and sloughing; in this way 
the cartilage of the nose may be destroyed, with sinking in of 
the bridge. In the viscera, the gummata may undergo fibro- 
sis, with puckering and deformity of the organ. The bone 
affections at this stage are marked by nocturnal pains. 

Sequelae. — Amyloid degenerations; sclerotic degenerations, 
such as locomotor ataxia; and arterio-sclerosis. 

Diagnosis. — The primary sore is distinguished from the chan- 
croid by the fact that the latter is usually pustular, is never 
indurated, is usually multiple, has no period of incubation, 
and is followed by no constitutional symptoms. Chancre of 
the lip has been mistaken for cancer, but the history, symp- 
toms, and therapeutic test will soon combine to settle the 
question. 

Various skin eruptions (psoriasis, lichen, papular eczema) 
may resemble the cutaneous syphilides; if the history and asso- 
ciated symptoms are insufficient for diagnosis, careful investi- 
gation will nevertheless disclose minor points of differentiation. 

The syphilitic arthritis which may develop at the onset of 
the second stage, and the pains of the tertiary stage, must be 
distinguished from rJicumatism and gout ; this is accomplished 
by a consideration of the history, the associated symptoms, 
and the therapeutic test. 

Prognosis. — Under proper treatment, good. As a rule re- 
covery is complete in from two and a half to three years. 

HEREDITARY SYPHILIS. 

Symptoms. — All of the lesions incidental to acquired syphilis, 
except the chancre, can occur in the victim of hereditary 
syphilis. In addition there is a tendency on the part of the 
mother to repeated abortions, the aborted fetus in each case 
being shriveled, with skin exfoliated, and evidently some time 
dead; and if, perhaps after a series of abortions, a viable child 



108 INFECTIOUS DISEASES. 

is borne, it is apt to be wizened, poorly developed, with bullse 
upon hands and feet (pemphigus neonatorum), fissured lips, 
and snuffles. The child may be apparently healthy at birth, 
but before the fourth month symptoms of the malady usually 
appear. Characteristic coppery patches, notched teeth, and an 
appearance of premature old age may be noted. Later, 
should the patient outlive his childhood, he is apt to be 
stunted, deformed, and undeveloped, appearing much younger 
than he really is — a condition of so-called infantilism. In ex- 
ceptional cases the symptoms of the disease are not dicovered 
until the age of puberty or even later. 

Diagnosis. — The appearance in a child of less than five 
months of snuffles and skin eruptions usually suffices for a 
diagnosis. 

Treatment. — Prophylaxis. The patient must be cautioned as 
to the danger of his infecting his associates, and every thing 
involving contact with others must be forbidden until treat- 
ment has been prolonged, and all symptoms have disappeared 
for a considerable time. If a woman develops syphilis while 
pregnant, active treatment must be begun at once and con- 
tinued after birth of the child. 

Primary stage. Excision of the chancre does not prevent 
constitutional infection and is therefore inadvisable. Dust the 
sore with aristol, bismuth subnitrate, or calomel; but unless 
diagnosis is positive, administer no internal medicines until 
unquestionable secondary manifestations appear. 

Secondary stage. Administer one grain of mercury binio- 
dide 2x or two grains of mercury protoiodide 2x three times a 
day, after meals; continue this, and if necessary increase 
the dose, until the symptoms yield. Then prescribe the 
"tonic" dose of half that amount until active symptoms again 
appear, when the dose must be increased immediately to its 
former size. Should the stomach rebel, resort to inunctions: 
use one-half drachm of mercurial ointment mixed with an 
equal quantity of vaseline, daily. Spend from 20 to 30 minutes 
in rubbing it into the skin, selecting a different part of the 



INFECTIOUS DISEASES. 109 

body for each inunction, — the axillae, the groins, the inside of 
the thighs, etc. The limit of toleration on the part of the 
patient is indicated by increased saliva, a blue line on the 
gums, colic, and diarrhea; the dose must be kept just below 
this action until the symptoms yield. 

During the period of active symptoms the patient must 
live a rational life, free from excesses of all kinds, and as far as 
possible he should be out of doors. His diet should be ample 
but easily digestible, daily or bi-weekly baths are beneficial, 
and he should have plenty of recreation. Smoking and chew- 
ing must be prohibited because of the tendency to lesions in 
the mouth; and the teeth must be kept in perfect order. 

Tertiary stage. The tertiary manifestations have a specific 
remedy in potassium (or sodium) iodide ; a saturated solution 
of this drug should be given, well diluted with water or milk, 
half an hour after each meal. The initial dose may be live 
drops three times a day, but this should be increased rapidly 
and if necessary to enormous quantities, in order to control 
the disease. Exceptionally the coincidence of skin and visceral 
symptoms will require the use of mercury and an iodide 
together (mixed treatment); in these cases it is well to give 
mercury by inunction and potassium iodide by the mouth. 

Hereditary syphilis is treated in the same way, the doses of 
medicine being, of course, adapted to the age of the patient. 



LEPROSY. 

(Lepra.) 

Etiology. — The exciting cause is the lepra bacillus, a minute 
rod closely resembling the tubercle bacillus. The disease is 
transmitted by contact, possibly only by inoculation, and gen- 
erally as an incident of sexual intercourse. 

Pathology. — 1. Nodular infiltrations (tubercles) appear upon 
the skin, projecting from its surface; and since they are poorly 
supplied with blood-vessels, they soon undergo caseation and 



110 INFECTIOUS DISEASES. 

either absorption or fibrosis, or else pyogenic infection leads 
to ulcerative and destructive changes. Similar lesions involve 
the mucous membranes and internal organs. 

2. Nodular infiltration of various nerve trunks leads to neu- 
ritis, at first attended by local hyperesthesia, but later leading 
to complete anesthesia together with trophic changes in the 
parts supplied by the affected nerve. The nerve trunk, in- 
filtrated with the leprous growth, may be felt as a thickened 
cord beneath the skin. 

Forms. — According to the predominance of one or the other 
of these lesions, two forms of leprosy are recognized, viz., the 
tubercular and the anesthetic. 

Symptoms. — The disease develops only after a prolonged 
incubation (3-5 years). In the tubercular form there appears 
at first a patchy redness of the skin which is slightly elevated 
and hyperesthetic. In a little while the redness and later the 
pigment disappear from the area, leaving it white and anes- 
thetic {lepra alba). Tubercular nodules develop in the skin, 
the smaller ones disappearing again but the larger breaking 
down into ulcers which finally cicatrize and occasion marked 
deformity. Similar ulcerations affect the mucous membranes 
of the nose and throat. 

In the anesthetic form the onset is marked by the develop- 
ment of painful hyperesthetic patches in the skin. Small 
bullae, representing trophic changes, appear on the arms and 
legs, and the muscles supplied by the affected nerves undergo 
atrophy. Red patches of vasomotor congestion appear and in 
turn become anesthetic, and finally only dry, scaly, whitish 
patches remain. The trophic changes may become extreme, 
the bullae bursting and leaving perforating ulcers, and as the 
result of atrophy and necrosis combined, great deformities 
may be produced, and fingers and toes may even drop off 
{lepra mutilans) . 

Diagnosis. — Patchy erythema with hyperesthesia, followed by 
local anesthesia and the appearance of characteristic nodules, 
affords unmistakable evidence of leprosy. Syringomyelia,) 



INFECTIOUS DISEASES. 



Ill 



the only disease notably similar, is dependent upon a central 
rather than a peripheral lesion; its symptoms are localized to 
an area enervated from one spinal cord segment rather than 
from a nerve-trunk, and the tactile sense is not lost as in 
leprosy. 

Prognosis. — The disease is hopeless, but the course is pro- 
longed, and the patient may live in comparative comfort for 
many years. Death finally occurs from exhaustion or some 
intercurrent disease. 

Treatment. — Symptomatic. 



THE PLAGUE. 

(Bubonic Plague; Black Death.) 

Etiology.— The exciting cause is a bacillus, a short rod with 
round ends which gains entrance to the body through the 
digestive or respiratory tracts or through breaks in the integu- 
ment. The organism is said to be conveyed by rats, and in- 
sanitary conditions predispose to the contagion. 

Symptoms. — The onset of the disease is attended with severe 
pains in the head, back, and limbs, and intense dizziness. 
Sometimes there is a slight chill, and the temperature rises 
rapidly to a high point. There is thirst, often nausea and 
vomiting, and early delirium. Petechia?, and in malignant 
cases hemorrhages from the mucous membranes, may be noted. 
If the patient does not succumb at the outset, on the second 
or third day the characteristic buboes appear, usually in the 
inguinal region; these ma} T reach the size of an egg, are very 
tender, and often rupture and discharge. Upon the appear- 
ance of the bubo, the fever subsides, with a profuse sweat to 
signalize the crisis. Carbuncles may also be present. 

Diagnosis. — Typhus fever presents a characteristic eruption 
and lacks the buboes, petechia?, hemorrhages, etc. 

Prognosis. — The prognosis is very grave, a large majorit3 T of 
those affected dying. Death may occur within a few hours, or 
life may be prolonged for a week or more. In favorable cases 



112 INFECTIOUS DISEASES. 

convalescence is protracted by the profuse suppuration which 
occurs. 

Treatment. — Prophylaxis is most essential; the infected in- 
dividuals must be isolated, disinfection must be thorough, and 
hygienic defects must be remedied. The treatment must be 
conducted on general principles, including fever diet, sympto- 
matic medicines, and antiseptic cleansing of the abscesses. 






DISEASES OF THE CIRCULA- 
TORY SYSTEM. 



In diseases of the circulatory system no definite relation 
between symptoms and physical signs exists. For example, 
the objective evidences of disease of the heart and arteries 
may be unmistakable while subjective symptoms are entirely 
absent. On the other hand, general symptoms may be domi- 
nant while the physical signs are slight or absent, as in angina 
pectoris. Finally, there are cases in which physical signs and 
subjective phenomena are closely associated, as in uncompen- 
sated mitral disease. 

The one important question in any disease affecting the 
circulatory apparatus is the condition of the heart muscle. 
No matter how apparent a valvular defect, there will be no 
disturbance in the circulation so long as the cardiac muscle 
can by hypertrophy compensate for the deficiency. Hence, in 
every case the physician must determine not only what part 
of the heart is diseased, but to what extent the heart muscle 
is able to keep up the general circulation. In short, it is to 
the indications of cardiac failure that attention is generally 
directed. The cardinal symptoms of this are those due to 
pulmonary congestion, evidenced by dyspnea, cough, hemopty- 
sis, or pulmonary edema ; and those due to back pressure in 
the inferior vena cava, leading to hyperemia of the liver y 
stomach, intestines, spleen, and kidneys ; and to general dropsy. 
Back pressure in the superior cava may induce cyanosis of the 
face and lips, and so little blood may be sent to the brain that 
vertigo or syncope is induced. These signs and symptoms 



114 DISEASES OF THE CIRCULATORY SYSTEM. 

indicate grave weakness of the heart muscle, whether a valvu- 
lar lesion be detectable or not. 

Interrogation of the Patient.— When attention is directed to the 
heart or blood vessels, it is important to ascertain if there be — 

1. A family history of gout, rheumatism, heart disease, 
Bright's disease, or paralysis of cerebral origin (hemorrhage, 
thrombosis, embolism). 

2. A personal history of rheumatic fever, chorea, scarlet 
fever, diphtheria, syphilis, and other infections. In children, 
inquire concerning sore throats and " growing pains.", 

3. Subjective sensations. Does he suffer with dyspnea. Can 
he sleep lying down, or must he sit up in bed ? Does he have 
any precordial pain or distress? What is its exact situa- 
tion and character? Does it radiate or not? If so, in what 
direction? Does he complain of palpitation? What is its re- 
lation to meals and to exertion ? Does the heart give an 
occasional thump? Is his sleep good or bad? Does he dream? 
Is vertigo ever present, and when ? 

4. Signs of venous stasis. Do the feet ever swell ? Has he 
a cough ? Is his digestion good ? Does his nose ever bleed ? 



PHYSICAL EXAMINATION OF THE PATIENT. 

Having placed the patient, stripped to the waist, in a good 
light, the observer should stand before him and systematically 
note the points elicited by inspection, palpation, percussion, 
and auscultation, concluding with an investigation of the pulse 
characteristics. 

Inspection and palpation are usually practiced together, the 
examining hand verifying the discoveries of the eye. 

1. Inspect the precordia, noting — 

Its form : is there any bulging over the precordia ? Is there 
any chest deformity which can displace the heart ? 

Its movements : note with the eye the apex beat, its situa- 
tion, force, and diffusion. Place the flat of the hand over the 
cardiac area, the fingers covering the apex region, and notice 



DISEASES OF THE CIRCULATORY SYSTEM. 115 

whether there is the normal moderate impulse, or the strong, 
heaving impulse of hypertrophy, the peculiar sudden tap of 
mitral stenosis, or the weak, perhaps imperceptible, slap of 
dilatation. Thrills and vibrations, systolic or presystolic, may 
be discovered at the same time. Note the position of the apex 
beat. Normally it is in the fifth interspace well within the 
nipple line; but hypertrophy of the left ventricle displaces it 
downwards, dilatation forces it outwards and downwards, and 
enlargement of the right ventricle pushes it outwards. Dis- 
placements may also be due to causes outside of the heart 
itself, such as pericardial adhesions, pleural effusion, etc., and 
these possibilities must be remembered. 

2. Note any epigastric pulsation. This may sometimes be 
due to hypertrophy of the right ventricle. 

3. Inspect the aortic region, noticing 

(a) Pulsation in the pulmonary area, often seen in anemia. 
(&) Pulsation in the aortic area, which may be seen and 
felt in cases of aneurism. 

4. Inspect the neck, noting 

(a) Fulness of the jugular veins. If there is distension of 
one side, it may be due to pressure (aneurism or tumor) on 
the innominate; if of both sides, it signifies either pressure on 
the superior rena cava or on both innominates, or dilatation 
and engorgement of the right heart. 

(&) Pulsation in the jugular veins, signifying tricuspid re- 
gurgitation following great dilatation of the right heart. 

{c) Excessive pulsation in the arteries, including the char- 
acteristic carotid throb below the ramus of the jaw which 
accompanies aortic regurgitation. 

5. Inspect the general circulation, evidence concerning 
which may be found in the patient's complexion, his peri- 
pheral arteries and veins, the presence or absence of dropsy, 
etc. 

Percussion verifies and extends the information gained through 



116 DISEASES OF THE CIRCULATORY SYSTEM. 

inspection and palpation. With its aid the examiner investi- 
gates: 

1. The area of superficial cardiac dulness. In health this is 
a small triangle whose internal border is formed by the left 
edge of the sternum, the external border being defined by a 
line running outward from the sternum along the lower level 
of the fourth cartilage nearly as far as its junction with the rib, 
and then dipping down and curving slightly outwards to the 
point of the apex beat. The lower border is lost in the liver 
dulness. 

2. The area of deep cardiac dulness, which corresponds 
approximately to the true dimensions of the heart, should be 
determined by firm percussion at the end of expiration. Per- 
cussion must be made at successive points along lines approach- 
ing the dull area at right angles, until a change of note is 
detected. 

The area of dulness may be extended to the left, passing the 
nipple line (dilatation of the left ventricle), to the right 
(dilated right ventricle), or in both directions and upwards as 
the result of pericardial effusion. In every case, however, it 
must be decided that there is actual enlargement, not dis- 
placement, of the heart, and not withdrawal of the adjacent 
lung, whereby a greater cardiac area lies against the chest. 

3. The region of the aorta lies above the third cartilage. Dul- 
ness in this situation is always abnormal (aneurism, tumor of 
mediastinum). 

Auscultation completes the examination of the heart itself, 
confirming or interpreting the evidence obtained by inspec- 
tion, palpation, and percussion. The ear may be applied 
directly to the chest, or the examiner may prefer to use a 
stethoscope. The points of greatest importance, each repre- 
senting the area at which the sounds produced at a certain 
valve are heard with greatest intensity, are four in number, 
viz. : 

1. The "mitral area" at the apex of the heart in the fifth 
left interspace near the nipple. 



DISEASES OF THE CIRCULATORY SYSTEM. 117 

2. The "pulmonic area" in the second left interspace near 
the sternum. 

3. The "aortic area" in the second right interspace near 
the sternum. 

4. The " tricuspid area" at the bottom of the sternum near 
the ensiform cartilage. 

At each of these the examiner listens in turn. In health he 
hears characteristic normal sounds at each point. In disease 
there may be alterations in the character of those sounds, or 
there may be in addition certain adventitious sounds due to 
diseased conditions about the valve which obstruct the flow of 
blood (stenosis), or allow it to leak backwards (insuf- 
ficiency, incompetency, or regurgitation). In the study of 
such an adventitious sound, called a murmur (bruit, souffle), 
five facts must be ascertained: 

(1) Its time of occurrence (during systole, during diastole, 
etc.). 

(2) Its point of maximum intensity. 

(3) The area over which it can be heard, i. e., its direction 
of transmission. 

(4) The effects of position, respiration, and exertion upon it. 

(5) Its character, whether blowing, rasping, musical, etc. 
Murmurs are loud in proportion to the force of the blood 

current, and therefore loudness is often a favorable sign, 
indicating a strong heart muscle. With dilatation and failure 
of compensation the murmurs, even though due to extensive 
lesions, may completely disappear. 

1. In the mitral area both heart sounds are audible in health, 
the first long and low pitched and the second short and sharp. 
It may be noted that the first sound is weaker than usual 
(myocardial degeneration or asthenia), or it may be louder, 
i. e. , accentuated; in the latter case it will be short and sharp 
if there is dilatation, prolonged and dull if there is hyper- 
trophy. Often the first sound is reduplicated, owing to lack 
of synchronism between the ventricles. The duration of the 



118 DISEASES OF THE CIRCULATORY SYSTEM. 

interval between the first and second sounds, indicating the 
length of cardiac systole, and that between the second and 
first, representing the cardiac diastole, should be noted. The 
systolic interval may be so shortened that the second sound 
follows the first almost without pause; this indicates incom- 
plete contraction of the ventricle and is often a grave sign, 
indicating impending heart failure. 

The murmurs heard at the apex may be systolic, pre-systolic, 
or diastolic. The systolic murmur is usually smooth and blow- 
ing, sometimes rumbling, and signifies regurgitation through 
the mitral orifice. The pre-systolic murmur, so-called because 
it precedes and runs up to the first sound, is usually vibratory 
in character and indicates, obstruction at the mitral orifice 
{mitral stenosis). If a diastolic murmur is heard at the apex 
it is usually one transmitted from the base. 

2. In the pulmonic area organic murmurs may be systolic 
{stenosis) or diastolic {regurgitation), but these affections are 
rare, generally congenital. A majority of the murmurs heard 
in the pulmonic area are functional or else are simply trans- 
mitted from their origin at the mitral or aortic orifices. Ac- 
centuation of the pulmonic second sound is usual in children; 
in adults it is generally pathological and points to obstruction 
to the pulmonic circulation (mitral disease, emphysema, etc.). 

3. In the aortic area there may be a systolic murmur, indi- 
cating stenosis, or a diastolic murmur significant of regurgita- 
tion. In addition, there may be accentuation of the aortic 
second sound as the result of any cause (arteriosclerosis, inter- 
stitial nephritis) which increases the resistance in the arterial 
system and so adds to the work of the left ventricle. 

4. In the tricuspid area systolic, pre-systolic, and diastolic 
murmurs may be heard. The two latter are usually trans- 
mitted from apex or base and cannot be relied upon for 
diagnostic purposes ; the systolic murmur may indicate tricuspid 
regurgitation. 

Functional {hemic) murmurs, not due to any organic lesion 
of valves or orifices, are common. They are usually systolic, 



DISEASES OF THE CIRCULATORY SYSTEM. 119 

mostly pulmonic, and are soft in character and not transmitted; 
they are remarkably evanescent, are unassociated with en- 
largement of the heart, and the patient is often anemic. 

Exocardial sounds, due to pericardial or pleural friction, 
are distinguished by the fact that they are peculiarly super- 
ficial and are not synchronous with the heart beat. The peri- 
cardial sound is often heard only at irregular intervals. The 
pleuritic sound ceases when the patient holds his breath. 

The Pulse. — It is customary to feel for the pulse in the radial 
artery simply because the wrist is most accessible; the facial 
or the temporal artery affords the same information and may 
be utilized occasionally. It is well to feel both radials at the 
same time, laying the tips of three fingers upon each artery. 
Note: 

1. The pulse rate. In healthy adults this varies between 60 
and 80; in children it is 100 or more. 

2. The pulse rhythm (regularity, irregularity). 

3. The amount of force necessary to obliterate the pulse 
{compressibility). To estimate this, gradually increase the 
pressure of the finger nearest the patient's heart until the 
pulse wave ceases to be felt by the other fingers. Experience 
is necessary in order to draw the proper conclusion. 

4. The extent to which the artery collapses between beats 
{tension). The pulse of low tension completely collapses 
between beats, but that of high tension is perceptible between 
beats as a distinct cord which can be rolled between the 
fingers. 

5. The state of the arterial walls. Flatten the vessel and 
cause the patient's skin to slip up and down over it; in health 
the vessel wall can scarcely be detected, but if it is diseased 
the thickening or tortuosity can be plainly felt. 

In order to secure a permanent record and to aid in the 
analysis of the pulse characteristics, the sphygmograph may be 
employed. 

The most convenient instrument for clinical use is that of 
Dudgeon. Slips of paper procured from the instrument maker 



120 DISEASES OF THE CIRCULATORY SYSTEM. 

or else carefully cut to fit the sphygmograph and prepared by 
smoking one surface in the fumes of camphor, should be placed 
in the holder which accompanies the instrument. Find on 
the wrist the exact spot where the radial pulse is most distinct 
and mark it with an aniline pencil. Let the patient take a 
comfortable position, with the elbow resting on some solid 
support,. such as the edge of a desk, and with the hand out- 
stretched, palm upward. Place the metal button which works 
the writing lever exactly on the mark over the radial artery, 
tighten moderately the strap which holds the instrument in 
place, and endeavor to begin with the minimum pressure 
that will give characteristic tracings. Place one of the pre- 
pared slips of paper between the rollers, start the clockwork, 
and either stop it again before the slip has quite run out or 
else catch the latter in the hand. It is well to take three or 
four tracings, varying the pressure each time by turning the 
regulating lever until the greatest amplitude of movement is 
secured. 

After the tracings have been made, mark with a pin-point 
on the smoked surface the name, date, etc., and dip the slip 
into a solution of gum benzoin, one ounce to six ounces of 
alcohol, and allow it to dry. It can then be preserved in- 
definitely. 

The normal pulse tracing exhibits a straight, nearly vertical 
upstroke ; a moderately acute apex ; a gradual descent ; a 
small tidal wave ; and a well-marked dicrotic wave. Varia- 
tions from this normal standard will occur in correspondence 
with changes in the force, volume, tension, and rhythm of the 
pulse ; but for their correct recording and interpretation ex- 
tended experience with the sphygmograph is necessary. 
The chief value of the instrument lies in the permanent record 
of the pulse characteristics which it furnishes. 






DISEASES OF THE CIRCULATORY SYSTEM. 121 

DISEASES OF THE PERICARDIUM. 
PERICARDITIS. 

Etiology. — Inflammation of the pericardium may be due to: 

1. The toxic products of infectious disease (rheumatism, 
pyemia, scarlet fever, typhoid fever, etc.). 

2. The accumulation of excrementitious matters in the blood 
(Bright's disease). 

3. The extension of inflammation from the adjacent struct- 
ures (pleurisy, tuberculosis, etc.). 

4. Traumatism (blows, wounds, fractured ribs). 
Pathology. — 1. Dry pericarditis. The pericardial membrane 

become hyperemic, its epithelium detached, and its surfaces 
spread with yellow flakes of inflammatory lymph. By the 
incessant contact and separation of these sticky surfaces the 
" shaggy" or "hairy" heart is produced. 

2. Pericarditis with effusion. Should the inflammatory 
process continue, an exudate of clear, straw-colored fluid is 
poured out and distends the sac. In favorable cases this is 
ultimately re-absorbed, leaving behind it adhesions between 
the pericardial surfaces. Rarely the exudate becomes puru- 
lent. 

Symptoms. — Pericarditis is usually secondary to other dis- 
eases, and in consequence its onset is insidious. The patient 
complains of pain or more often discomfort in the region of 
his heart, and dyspnea. There is moderate fever (below 103°), 
the pulse becomes frequent, and there may be tenderness on 
pressure over the heart. As the effusion accumulates and op- 
presses the heart, the latter becomes irregular or intermittent, 
its second sound may be reduplicated, and during inspiration 
the pulse may become feeble or even cease {pulsus para- 
dox icus). 

Physical Signs. — 1. Dry stage. Pericardial friction, a rough 
"to and fro" murmur, heard irregularly during the greater 



122 DISEASES OF THE CIRCULATORY SYSTEM. 

part of each cardiac cycle and increased in intensity by the 
pressure of the stethoscope. 

2. Stage of effusion, (a) Extension of the area of cardiac 
dulness to both sides and upwards, forming a pyramid with its 
base in the nipple line and its apex about the first rib. 

(b) Disappearance of the friction sound, with progressive 
muffling of the heart sounds, the latter disappearing first at the 
apex and last at the aorta. 

(r) Obliteration of the intercostal spaces in the precordia, 
while the apical impulse becomes diminished or lost. 

3. Adherent pericardium can rarely be diagnosed during life 
unless there are in addition adhesions to the chest wall or the 
adjoining pleura. In such cases the heart may be enlarged, 
and its apex fixed so that it does not alter its position during 
respiration or on change of posture; there may be retraction 
of the chest wall during systole, and on palpation a diastolic 
shock may be felt. 

Diagnosis. — The friction sound of pleurisy is synchronous 
with the respiratory movements. Endocardial murmurs are 
less superficial and are not increased by pressure of the 
stethoscope. In dilatation of the heart the sounds are weak 
rather than distant or muffled, and venous stasis is more pro- 
nounced. If it is suspected that the pericardial effusion has 
become purulent, diagnosis can be rendered positive by the 
use of the exploring needle. 

Prognosis. — Death rarely occurs, and uncomplicated cases 
may recover within three weeks. Pericardial adhesions may 
permanently cripple the heart, however. 

Treatment. — Place the patient at rest, and apply hot poul- 
tices or ice-bags to mitigate the pain if it is severe. During 
the dry stage, spigelia is usually indicated, though aconite or 
cannabis may be preferred. When effusion occurs, arscnicum, 
bryonia, cantharis, or mercurius corr. should be given, accord- 
ing to the indications. Digitalis may be required by a weak 
heart, and potassium iodide may be given to promote absorp- 
tion of the exudate. If the effusion is so great as to embarrass 



DISEASES OF THE CIRCULATORY SYSTEM. 



123 



the heart's action, aspirate in the fifth interspace about one 
inch to the left of the sternum. 

Hydropericardium (serous accumulation in the pericardium) 
may occur as the result of obstruction to the veins of the heart 
by valvular lesions or pulmonary disease, or simply as part of 
a general dropsy. Its physical signs are those of pericardial 
effusion, but it is not accompanied by fever. 

Hemopericardium (blood in the pericardium) may result from 
rupture into the sac of an aneurism, rupture of the heart itself, 
or wounds of the heart. It is quickly fatal. 

Pneumopericardium (air or gas in the pericardium) is a rare 
condition, usually the result of traumation (stab wounds) or 
perforation by a foreign bod}'. Fluid and usually pus are also 
present, leading to peculiar splashing sounds. It is rapidly 
fatal. 



DISEASES OF THE ENDOCARDIUM. 
ENDOCARDITIS. 

Etiology. — The disease is invariably due to infection of the 
endocardial membrane, the organisms being those of rheuma- 
tism, chorea, diphtheria, scarlet fever, tuberculosis, cancer, 
etc. Chronic valvulitis predisposes to recurrent acute in 
fection. 

Pathology. — As a rule the inflammation is confined to the 
valves (valvulitis), although the lining of the cavity may be 
involved (mural endocarditis). In adults the left side of the 
heart is usually the one affected; in embryonic life it is the 
right. The infected valve becomes covered with small grayish 
patches, "vegetations," consisting of fibrin and leucocytes de- 
posited on a base of granulation tissue. The latter becomes 
organized and later undergoes cicatricial contraction, so that 
the valves become puckered and mis-shapen and sometimes 
glued together at their margins (chronic valvulitis). Less 
often the lodgment of pyogenic organisms leads to necrosis, 



124 DISEASES OF THE CIRCULATORY SYSTEM. 

with the formation of ulcers. In any case vegetations are 
liable to be broken off and carried away in the circulation to 
lodge elsewhere as emboli. 

Symptoms. — These are to a great extent masked by the pre- 
existing disease, of which endocarditis is but a part. The 
occurrence of dyspnea, precordial oppression, a quickened and 
perhaps irregular pulse, and a slight rise of temperature, may 
lead the attendant to suspect the onset of endocarditis. 

Physical Signs. — A murmur, most often heard in the mitral 
but sometimes in the aortic area, is alone conclusive. Its ap- 
pearance may, however, be preceded by some alteration in 
the first sound (prolongation or reduplication). 

Forms. — 1. Acute simple endocarditis, the benign form, which 
is attended with warty vegetations. 

2. Infective endocarditis (ulcerative, diphtheritic, or my- 
cotic), the malignant form in which septic infection of the 
valves occurs. In this the valvular phenomena are accompa- 
nied by chills, sweats, cutaneous emboli, and other septic symp- 
toms, a typhoid state develops, and the patient usually dies. 

3. Chronic endocarditis, comprehending a majority of the 
chronic valvular defects. 

Diagnosis. — In the course of any infectious disease the heart 
should be examined frequently for evidences of endocarditis. 
The simple form is recognized by the history and physical 
signs, not by the symptoms. Infective endocarditis may be 
distinguished from the simple form by its septic temperature 
and symptoms, and in doubtful cases the blood may be exam- 
ined for pyogenic organisms and for the evidences of 
leucocytosis. In pericarditis the rub is heard only in the 
precordia, is very superficial, and is intensified by the pressure 
of the stethoscope. Functional murmurs are usually basic and 
are not attended by circulatory disturbance. 

Prognosis. — In the simple form death is rare, but generally 
the heart is damaged to an extent that can be estimated only 
after inflammation has subsided and compensatory changes 



DISEASES OF THE CIRCULATORS SYSTEM. 125 

have developed. In the infective form the outlook is very 
grave, few cases recovering. 

Treatment. — Place the patient at rest between blankets and 
limit the diet to nourishing liquids, avoiding an excess of 
fluid. Warm baths may be given, and pain may require the 
application of heat or cold to the precordia. In the early 
stage, aconite, veratrum viride, or spigelia may be given; and 
if these prove unsatisfactory, iodine or spongia should be con- 
sidered. Bryonia is useful in many rheumatic cases, and bella- 
donna in children. Alcoholic or other stimulants are required 
in moderation when circulatory failure threatens. As the 
attack subsides, such remedies as aumni, graphites, iodine, 
kali iod., and sulphur may be given in order to lessen the ex- 
tent of the damage to the valves. In the infective form the 
principal remedies are arsenic, crotalus, lachesis, and secale. 



CHRONIC VALVULAR DISEASES OF THE HEART. 

Etiology. — The majority of these lesions are the result of 
endocarditis, but occasionally the defect is due to atheroma- 
tous or calcareous degeneration, as when a chronic sclerotic 
process extends down the aorta and involves the aortic valves. 
Syphilis is often an important factor, while muscular strain, 
such as that induced by heavy lifting, is a rare cause. In 
many cases the valve-leaflets remain perfectly normal, but 
as a result of dilatation of the cavities the orifices become 
so enlarged that the cusps cannot meet across the opening, 
and so-called "relative insufficiency" ensues. 



MITRAL INSUFFICIENCY. 

Pathology. — In this, the most frequent of valvular lesions, the 
valve leaks and permits the blood to flow back into the left 
auricle during systole. In consequence the left auricle, unable 
to resist this backward flow, dilates. Then the blood, backing 
up in the pulmonary circulation and engorging the lungs, 



126 DISEASES OF THE CIRCULATORY SYSTEM. 

throws increased work on the right ventricle and the latter 
hypertrophies. This may suffice to restore compensation for 
a time, but finally the right ventricle undergoes dilatation, the 
tricuspid valve becoming relatively insufficient, and the right 
auricle and the general venous system become engorged, with 
resulting symptoms of stasis (dropsy, and passive congestion 
of the stomach, liver, kidneys, and other abdominal viscera). 
Physical Signs. — 1. A blowing, rasping, or musical murmur, 
entirely or partially replacing the first sound of the heart, is 
heard at the apex and frequently also in the fifth interspace 
toward the axilla and at the posterior border of the scapula. 
The pulmonic second sound is sharply accentuated, the aortic 
less so. 

2. In proportion to the accompanying enlargement of the 
heart the apex is pushed outward and downward, and the area 
of dulness is extended in the same direction. 

3. The pulse becomes irregular both in rhythm and force. 



MITRAL STENOSIS. 

Pathology. — This lesion occurs most often in women (75%), 
especially in the tuberculous, and is frequently combined with 
mitral regurgitation. The valve-leaflets may coalesce, form- 
ing a funnel; or by their cicatricial contraction a mere slit — a 

button-hole " orifice — may be left. In either case the blood 
is restrained from passing into the left ventricle, hypertrophy 
and dilatation of the left auricle ensue, and this is followed by 
the series of changes in the right heart and venous system which 
have already been described as the result of mitral insuffi- 
ciency. 

Physical Signs. — 1. A prolonged, grinding murmur, sharply 
localized to the apex or just above it, is heard during diastole 
or just preceding systole, i. e., presystolic, and terminates 
abruptly in a sharp first sound. This murmur is never 
functional. The pulmonic second sound is accentuated and 
often reduplicated. 



DISEASES OF THE CIRCULATORY SYSTEM. 



127 



2. A presystolic thrill is felt by the hand placed over the 
apex. 




Fig. 13- 



-Pulse Tracing from a Marked case of Mitral Stenosis. 
Kaltever. ) 



(Salinger- 



3. The pulse is not altered when stenosis is moderate; when 
it is extreme, the pulse becomes small from lack of blood, and 
when compensation fails it becomes irregular. 



AORTIC INSUFFICIENCY. 

Pathology. — This lesion, the most frequent cause of sudden 
death from heart disease, occurs next in frequency to mitral 
insufficiency, and is often combined with aortic stenosis. Its 
cause may be endocarditis, but more often it is arteriosclero- 
sis, the disease creeping down the aorta and involving the 
valve-leaflets. As a result the valve does not close properly, 
the blood flowing back into the left ventricle during systole. 
The left ventricle, endeavoring to restore the balance, hyper- 
trophies until the heart becomes enormous in size {bovine 
heart). Ultimately the tremendous pressure leads to incom- 
petency of the mitral valve, which is followed by the results 
already described. 




Fig. 14 — Pulse Tracing From a Case of Aortic Insufficiency. (Eichhorst.) 

Physical Signs. — 1. A diastolic murmur, of variable characters 
is heard in the aortic area and transmitted down along the 
sternum. 



128 DISEASES OF THE CIRCULATORY SYSTEM. 

2. Extension of the area of dulness and displacement of the 
apex downward and somewhat outward accompanies the 
hypertrophy. 

3. A ''water-hammer" (Corrigan's) pulse, in which the 
artery fills quickly but collapses immediately, is present. In 
addition there is violent arterial pulsation all over the body, 
most visible in the carotids. 



AORTIC STENOSIS. 

Pathology. — The valve cusps may be thickened and inelastic, 
so that they cannot fall back out of the way of the blood cur- 
rent, or they may be glued together, so that they obstruct the 
flow of blood. As a result the left ventricle hypertrophies, 
though not so enormously as in cases of aortic regurgitation, 




Fig. 15 — Pulse Tracing From a Case of Aortic Stenosis. (Eichhorst. ) 

and the sequential changes are the same. Uncomplicated 
aortic stenosis is the least common of valvular affections of the 
left heart, the lesion occurring more often in combination 
with aortic insufficiency. 

Physical Signs. — 1. A systolic murmur is heard in the aortic 
area and transmitted up into the arteries of the neck. This 
murmur is not pathognomonic of stenosis; it may be due to 
(1) anemia, (2) mere roughening or impaired flexibility of the 
valve, (3) acute or sub-acute aortitis, in which it is associated 
with substernal pain and heart failure (angina pectoris?), or 
(4) dilatation of the aorta just above the valves. 

2. Enlargement of the left heart is demonstrable by per- 
cussion and by palpation of the apex. 

3. The pulsus tardus, slow in reaching its maximum, small 
and frequent, but regular, accompanies aortic stenosis. 



DISEASES OF THE CIRCULATORY SYSTEM. 



129 



TRICUSPID INSUFFICIENCY. 

Pathology. — This lesion is rarely primary, and if so it is usually 
congenital. As a rule it is a relative insufficiency, accompany- 
ing the dilatation of the right ventricle which is caused by 
back pressure through the lungs, and it leads to general 
venous stasis. 

Physical Signs. — 1. A systolic murmur, heard with greatest 
intensity about one-third of the distance between the left edge 
of the sternum and the nipple line, indicates tricuspid regurgi- 
tation. It is usually audible about the apex and may be mis- 
taken for a mitral murmur. 

2. The veins of the neck appear distended, often pulsating, 
and frequently they will fill from below when emptied by 
pressure. 

3. The liver is congested and much enlarged, and may 
pulsate. 

TRICUSPID STENOSIS. 

Pathology and Physical Signs. — This rare lesion occurs in associa- 
tion with mitral stenosis, and is accompanied by a pre-systolic 
murmur heard in the tricuspid area and with difficulty distin- 
guished from that of mitral stenosis. If the lesion causes con- 
siderable obstruction, symptoms of venous back-pressure 
ensue; and the latter, occurring early in a case of mitral steno- 
sis, justify a suspicion of complicating tricuspid stenosis. 

PULMONIC VALVE LESIONS. 



Pulmonic Insufficiency occasions a diastolic murmur heard in 
the pulmonic area and transmitted downwards. It causes no 
special symptoms. 

Pulmonic Stenosis is nearly always congenital and gives rise to 
a loud systolic murmur which is conducted along the branches 



130 DISEASES OF THE CIRCULATORY SYSTEM. 

of the pulmonary artery over the entire chest. It is often 
associated with other congenital defects, notably a patent 
foramen ovale ; in the latter condition cyanosis is usually 
present. 

Diagnosis. — In the clinical study of valvular disease the fol- 
lowing points must be considered: 

1. The valve affected, and the relative danger attendant 
upon that particular lesion. For example, the liability to 
sudden death from aortic regurgitation is well known; of the 
other lesions, stenosis is usually more serious than a corre- 
sponding degree of regurgitation. 

2. The origin of the lesion, whether in rheumatic or other 
endocarditis, or in degenerative changes, etc. The lesions 
due to endocarditis, occurring in the comparatively young, 
may be compensated for by hypertrophy; with degenerative 
lesions this is much less likely to occur. 

3. The actual condition of valve and orifice, i. e., the extent 
of obstruction or amount of regurgitation. This may be indi- 
cated by its effect on the heart, i. e., by the degree of dilata- 
tion or hypertrophy induced. 

4. The nutritional soundness and functional vigor of the 
heart muscle and of the body in general, in order to judge as 
to the extent and time during which compensation can be 
depended upon. 

Prognosis. — The foregoing details, a knowledge of which is 
necessary to the proper diagnostic appreciation of a case, may 
be utilized in framing a prognosis, which implies consideration 
of— 

1. The lesion, including 

a. Its site and variety, with the relative danger attaching 
thereto. 

b. Its extent. 

c. Its character, whether progressive or stationary. 

2. The patient, including 

a. His nutrition, cardiac and general. 

b. His age. 



DISEASES OF THE CIRCULATORY SYSTEM. 131 

c. His family history, especially if there be hereditary 
tendency to heart disease. 

d. His habits and surroundings. 

e. The presence or absence of other diseases. 
Treatment of Chronic Valvular Disease. — While compensation re- 
mains complete the physician should content himself with 
prescribing such hygienic regulations as the individual re- 
quires. If nutrition is good, allow as much gentle exercise in 
the open air as possible. The diet should be liberal, but 
stimulants must be taken only in moderation. A warm 
climate at a moderate elevation affords a desirable resort for 
these patients. They should be protected from exposure, and 
constipation must be avoided. 

When symptoms of failing compensation are discovered, 
the patient must be put at rest, and a remedy prescribed 
in accordance with symptomatic indications. If these 
measures prove insufficient, then tincture of digitalis (gtt. 
ij — x t. i. d. ) or one of its substitutes, such as cactus, caffein s 
convallaria, spartein, or stropJianthus, must be prescribed. 
Should dropsy be present and persist in spite of these reme- 
dies, give calomel in doses of one-tenth grain every two hours 
for several days, or the infusion of apocynum or of digitalis, 
in doses of twenty drops or more every three or four hours. 
Sudden heart failure should be treated by rest, the application 
of heat to the precordia, and the hypodermatic use of glonoin 
2x, gtt. i. — ij, or strychnine, gr. -^V - 3V 

After urgent symptoms have been relieved, it is well to 
resort to such remedies as arsenic, arsenic iodide, or strych- 
nine to sustain the heart. 



DISEASES OF THE MYOCARDIUM. 

HYPERTROPHY OF THE HEART. 

Etiology. — An increase in thickness of the heart muscle is in- 
variably the result of increased activity of that organ, which 
may be induced by : 



132 DISEASES OF THE CIRCULATORY SYSTEM. 

1. Obstruction within the heart (valvular diseases). 

2. Obstruction outside the heart (aneurism, arterio-sclerosis, 
chronic nephritis, pericardial adhesions, etc.). 

3. Long-continued functional activity induced by laborious 
exercise, athletics, prolonged tachycardia of nervous origin, 
etc. 

Pathology. — When the cause lies at the aortic valve or out- 
side the heart, the left ventricle is the portion hyper- 
trophied; and in consequence this is the more frequent lesion. 
The right ventricle becomes involved when the obstruction 
lies at the mitral valve, in the pulmonary circuit, or in the 
right heart itself. The weight of the organ, normally about 
12 ounces in men and 10 }4 in women, may become greatly 
increased as the result of added thickness of the walls. This 
increase in bulk is due to the development of new muscle 
fibres (numerical hypertrophy). Hypertrophy may occur 
without enlargement of the cavities (simple hypertrophy) or 
hypertrophy and dilatation may co-exist (eccentric hyper- 
trophy). 

Symptoms. — Hypertrophy is a compensatory process and 
occasions few symptoms. Occasionally a patient complains of 
precordial discomfort or actual pain, palpitation, and pulsation 
in the head or neck. 

Physical Signs. — Hypertrophy of the left ventricle is indicated 
by an apex beat situated below the normal point and heaving 
in character, together with extension of the percussion dul- 
ness downward and to the left. The aortic second sound 
is louder than normal, but the first sound at the apex is duller. 
If the latter becomes prolonged, muffled, and "murmurish," 
careful auscultation is apt to show that it is reduplicated, thus 
revealing a tendency to dilatation. 

Hypertrophy of the right ventricle is evidenced by displace- 
ment of the apex outward rather than downward, with exten- 
sion of percussion dulness to the right of the sternum, and 
sharp accentuation of the pulmonic second sound. 

Diagnosis. — By the physical signs. 



DISEASES OF THE CIRCULATORY SYSTEM. 133 

Prognosis. — The only question is whether the hypertrophy 
has established adequate and durable compensation. It is 
adequate when no circulatory symptoms or distress on exer- 
tion remain. Impending failure of compensation may be 
indicated by a prolonged interval between the first and second 
sounds or by reduplication of the first sound. 

Treatment. — Since hypertrophy" is a conservative process, no 
direct treatment is required. The causative lesion should be 
controlled as far as possible. 

DILATATION OF THE HEART. 

Etiology. — Enlargement of the cavities of the heart may be 
due to — 

1. Sudden over-distention, induced by excessive exertion or 
valvular deficiency {simple dilatation). This is usually fol- 
lowed by hypertrophy of the walls {dilatation with hyper 
trophy). 

2. Thinning of the walls, owing to faulty nutrition. This 
represents the final stage, hypertrophy and the resulting com- 
pensation having failed. 

Pathology. — The muscular tissue undergoes inflammatory or 
degenerative changes, as a result of which the wall becomes 
thinned and inelastic, and in consequence it is unable to cope 
with an increase of blood pressure, and dilatation of the 
cavities results. When nutrition can be maintained or re- 
stored, a compensatory thickening of the walls may follow; 
but when nutritional failure has ensued upon a previous com- 
pensatory hypertrophy the muscle rarely becomes competent 
again. As a rule, more than one of the cavities is enlarged, 
and stretching of the valvular orifices often gives rise to rela- 
tive insufficiency. The left auricle and right ventricle are the 
cavities most frequently involved. 

Symptoms. — The dilatation ma}' be acute, the result of heart 
strain from over-exertion, or occurring in the course of an 
acute infectious fever. The symptoms are apt to consist of 
sudden pain about the heart, a rapid, feeble pulse, faintness, 



134 DISEASES OF THE CIRCULATORY SYSTEM. 

and dyspnea. This attack may be followed immediately by 
death; if not, the symptoms may pass off while the patient is 
at rest, but until compensation is established they tend to re- 
appear on the slightest exertion. 

In the more chronic condition resulting from a gradual loss 
of compensation, the symptoms are usually those of general 
venous stasis (dropsy), together with feeble pulse, dyspnea, 
palpitation, and sometimes anginal attacks. 

Physical Signs. — The apex is displaced and the area of per- 
cussion-dulness extended as in the case of hypertrophy, but the 
impulse is diffused and weak. The apical first sound is short 
and the aortic second sound is enfeebled. The interval be- 
tween the first and second sounds may be lengthened, or if 
failure is imminent it may be shortened, owing to incomplete 
contraction of the ventricle. Pre-existing murmurs may dis- 
appear, and on the other hand a mitral systolic murmur, due to 
relative insufficiency, may be heard. 

Prognosis. — Recovery from acute dilatation is possible; the 
chronic form is ultimately fatal. 

Treatment. — Rest, a light nutritious diet, and the administra- 
tion of heart tonics as directed for the general treatment of 
valvular disease, of which this is but a final stage. 

ACUTE MYOCARDITIS. 

Etiology. — Acute inflammation of the heart muscle is usually 
associated with peri- or endocarditis, and is due to the same 
causes, e. g., infectious diseases. 

Pathology. — The muscle fibres undergo changes varying from 
cloudy swelling to granular degeneration, while the connective 
tissue becomes proliferated. In connection with pyemia the 
process may be suppurative, the heart substance becoming in- 
filtrated with pus. The consequent weakening of the myocar- 
dium leads to acute dilatation (q. v.). 

Symptoms and Physical Signs. — These are indicative of progress- 
ive dilatation and asthenia, the latter being evidenced by 



DISEASES OF THE CIRCULATORY SYSTEM. 135 

feebleness or loss of the apex beat, and a rapid, easily com- 
pressible pulse. 

Prognosis.— This varies with the extent of the process. The 
milder cases recover ; the more severe may recover after pro- 
longed convalescence, but sudden death from slight exertion 
is not unusual. Suppurative cases rarely recover. 
Treatment. — That of the causal disease. 

CHRONIC MYOCARDITIS. 

(Fibrous Myocarditis; Fibroid Degeneration.) 

Etiology and Pathology. —As the result of disease of the coronary 
arteries the blood supply to the heart becomes diminished, and 
ultimately impaired nutrition leads to disappearance of the 
muscle fibres, which are replaced by connective tissue. The 
process may be diffuse or circumscribed. 

Symptoms and Physical Signs. — These are identical with those of 
dilatation of the heart. A slow pulse and anginal attacks are 
common. 

Diagnosis. — This is often difficult. The absence of a history 
of valvular disease, the existence of arterio-sclerosis elsewhere, 
and the occurrence of bradycardia and anginal attacks suggest 
fibroid degeneration. 

Prognosis. — Grave. 

Treatment. — Rest, nourishment, and the use of such drugs as 
cliloride of gold, iodide of arsenic, etc. Syphilitic cases should 
receive mercurius biniod. or kali iod. Digitalis and other 
heart-whips are of little value. 

DEGENERATIONS OF THE HEART MUSCLE. 

Parenchymatous or albumenoid degeneration (cloudy swelling) 
occurs in infectious fevers and as a first stage of fatty de- 
generation. 

Fatty degeneration (fatty metamorphosis, yellow atrophy) 
consists of a metamorphosis of the muscle-protoplasm into 



136 DISEASES OF THE CIRCULATORY SYSTEM. 

fat; it may be circumscribed, occurring in small foci, or gen- 
eral, as in dilatation of the heart succeeding hypertrophy. It 
is not recognizable during life. Death is liable to come sud- 
denly. When the disease is suspected, the general treatment 
should be that of dilatation, together with such remedies as 
arsenic, aurum, iodine, kalmia, and phosphorus. 

Fatty infiltration consists of a deposit of fat between the 
muscle fibres. It occurs as a part of general obesity, to which 
treatment should be directed. 

Atrophy of the heart consists of a wasting of the muscle sub- 
stance and a reduction in the size of the cavities. It develops in 
the course of wasting diseases, such as tuberculosis and cancer. 
Brown atrophy consists of a similar wasting in which the heart 
muscle becomes pigmented; its causes are the same, and in 
addition it occurs in connection with senile marasmus and 
chronic valvular disease. 

Amyloid degeneration may take place in the heart as it does in 
the other viscera. 



NEUROSES OF THE HEART, 

PALPITATION. 

Etiology. — The subjective sensation of forcible or rapid beat- 
ing of the heart may be due to: 

1. Emotional causes, such as joy, sorrow, or fright. 

2. Neurasthenic conditions, the result of overwork, excesses, 
etc. 

3. Toxic causes, including the over-use of tea, coffee, to- 
bacco, and alcohol. 

4. Reflex conditions in the stomach and other viscera. 
Symptoms. — The patient complains of violent beating of the 

heart, and on examination its action is often found to be rapid 
and forcible. In addition he may have sensations of flutter- 
ing and faintness, and there may be pain of anginal character. 
Diagnosis.— The diagnosis, which is usually easy, rests upon 



DISEASES OF THE CIRCULATORY SYSTEM. 137 

the exclusion of an organic cause for the symptoms. Search 
should also be made for the etiologic factors mentioned. 

Treatment. — Rest, the application of cold or heat to the pre- 
cordia, and therapeutic measures directed to the cause. 

TACHYCARDIA. 

Rapidity of the heart, the beat ranging from 100-200 or 
more per minute, may be symptomatic of many conditions, 
including various neuroses and lesions of the central nervous 
system, of the sympathetic system, and of the pneumogastric 
nerve. The tachycardia may be continuous or paroxysmal, 
and various subjective sensations may accompany it. In every 
case search should be made for the cause, whether it be a 
lesion of brain, cord, or thoracic viscera, or exophthalmic 
goitre, hysteria, or other neuroses. 

BRADYCARDIA. 

Unnatural slowness of the pulse, 60-10 or less, is often a 
symptom of serious degenerative change in the myocardium 
or aorta. Pulmonary, digestive, and renal disorders, toxic 
agents, and various lesions involving the medulla or cord, may 
also induce bradycardia. The beats should be counted while 
listening over the heart, for in some cases of ventricular 
failure every pulsation does not appear in the radial artery . 
The discovery of bradycardia should lead to a search for the 
cause, to which treatment must be directed. 

ARHYTHMIA. 

Cardiac arhythmia may be limited to simple irregularity of 
action, or there may be actual intermission, the heart drop- 
ping a beat at intervals. In the latter case it is important to 
determine whether the systole is omitted, the first sound being 
absent, or whether it is simply weak, not sending the pulsa- 
tion to the wrist. Arhythmia may be the result of myocardial 
weakness, but more often it is reflex or neurotic. Extreme ir- 



138 DISEASES OF THE CIRCULATORY SYSTEM. 

regularity is known as delirium cordis. Embryo car di a {fetal 
rhythm) is distinguished by a beat in which the long pause is 
shortened and the character of the first sound modified, so that 
the two sounds are alike and follow each other like the ticking 
of a watch. It is an alarming symptom, indicating extreme 
cardiac dilatation or asthenia. " Gallop rhythm" is character- 
ized by a reduplication of the first or second sound, so that the 
heart sounds resemble the footfalls of a cantering horse ; it is 
sometimes of serious import, especially in chronic nephritis. 
The bi- or trigeminal pulse is so called because of separation of 
the beats into groups of two or three ; it occurs in many heart 
affections, especially mitral disease. 

ANGINA PECTORIS. 

(Stenocardia; Neuralgia of the Heart.) 

Angina pectoris is a term applied to certain paroxysms of 
heart pain or discomfort which occur as symptoms of various 
lesions more or less grave. 

Etiology and Pathology. — Angina pectoris appears to be related 
to a number of degenerative lesions, especially obstruction of 
the coronary arteries from atheroma or thrombosis, myocar- 
dial degeneration, aortitis, and arterio-sclerosis. Its exact 
nature is unsettled; it has been ascribed to spasm of the heart 
muscle, to- a general vascular spasm, and to a neuritis of the 
cardiac plexus. 

Symptoms. — The paroxysm may be excited by exertion or 
emotion, but often occurs without apparent cause, even awak- 
ening the patient from sleep. The typical attack presents 
two striking symptoms, viz., 

1. Pain in or about the heart, frequently radiating into the 
left shoulder or arm. The character of this pain varies; in 
some cases it is mere discomfort, but in others it is an inde- 
scribable agony, as if the heart were being gripped by an iron 
claw and torn from the chest. 

2. A horrible sense of impending death. The patient stands 



DISEASES OF THE CIRCULATORY SYSTEM. 139 

motionless, not daring to move or breathe; his eyes are star- 
ing, his face bathed in a clammy sweat, and he feels as though 
every moment were his last. 

The duration of the paroxysm varies from a few seconds to 
several minutes. At its conclusion there is usually an eructa- 
tion of gas from the stomach, to the presence of which the 
patient frequently attributes the attack. Occasionally he 
vomits or passes large quantities of pale urine. 

Forms. — -An attempt has been made to distinguish — 

(1) Angina pectoris vasomotoria, characterized by a spas- 
modic contraction of the cardio-vascular system; (2) angina 
pectoris gravior, in which cardio-vascular spasm is associated 
with a diseased heart; and (3) primary cardiac angina, in 
which the diseased organ is itself the seat of the disturbance. 
In addition, a pseudo-angina of neurotic origin is described. 
Clinically it is impossible to distinguish clearly between these 
varieties of heart pain. 

Diagnosis. — The typical attack is easy of recognition; but if 
either the pain or the sense of impending dissolution is absent 
or not characteristic in degree, doubt must be felt as to the 
gravity of the seizure. As a rule, a high tension pulse, con- 
tracted during the paroxysm, indicates grave ("true") 
angina. The first attack is, moreover, almost invariably ex- 
perienced during exertion. The attack of pseudo-angina in a 
neurotic patient is often prolonged and attended with rest- 
less excitement and hysterical symptoms. Gastralgia usually 
appears when the stomach is empty, the pain does not radiate 
to the shoulder or arm, the sense of impending death is absent, 
and heart disease is not necessarily associated with it. 

Prognosis. — Recovery after typical attacks of angina is possi- 
ble, but rare ; death is common in the second or third attack. 
It is impossible to frame an accurate prognosis, but the co- 
existence of marked cardio-vascular degeneration renders the 
outlook dark. 

Treatment. — The paroxysm requires the prompt use of amy I 
nitrite, a few drops being inhaled from a handkerchief, or one 






140 DISEASES OF THE CIRCULATORY SYSTEM. 

*or two drops of glonoin 2x may be placed on the tongue. In- 
halations of chloroform or ether and the hypodermatic use of 
morphia are also recommended. Between paroxysms treat- 
ment should be directed to the conditions found in heart or 
arteries. Arterio-sclerosis suggests gout or syphilis, and the 
discovery of either of these causal factors affords a basis for 
treatment. The patient must avoid immoderate exercise and 
emotional excitement, must take small, frequent and nourish- 
ing meals, and must avoid constipation. Among the more 
important medicines are arsenic, mix vomica, and phosphorus ; 
indications may also be found for aconite, anrnm, belladonna^ 
cactns, kali iod., spigelia, and many other remedies. 



DISEASES OF THE BLOOD VESSELS. 
ARTERIO-SCLEROSIS. 

(Endarteritis; Atheroma; Arterio-capillary Fibrosis.) 

Etiology. — 1. Old age. Senility is essentially a condition of 
arterio-capillary degeneration. 

2. The presence in the blood of toxic substances, due to 
gout or its causes, such as over-eating and drinking and lead 
poisoning, to chronic nephritis, and to syphilis. 

3. Excessive work combined with faultv nutrition and hy- 
giene. 

4. Heredity. 

Pathology. — The sclerotic changes occur most frequently in 
the wall of the aorta; the coronary arteries and the other 
large arteries are also commonly involved. The disease may 
be circumscribed or diffuse. 

1. Circumscribed arterio-sclerosis. In this form the intima, 
which normally is smooth, exhibits localized areas of thicken- 
ing, yellowish-white in color, which may ultimately undergo 
softening and disintegration (athermatous abscess). The dis- 
ease begins as a localized infiltration of the outer coats of the 
vessel, the connective tissue hyperplasia in the intima being 



DISEASES OF THE CIRCULATORY SYSTEM. 141 

a compensatory process. These areas ma} 7 become disinte- 
grated before thickening of the intima has supervened, and 
local dilatation is the result. 

2. Diffuse arteriosclerosis. In this form, which is often 
associated with circumscribed athermatous patches in the 
aorta, the intima appears smooth, but microscopic examina- 
tion reveals great thickening of it and the other coats with 
connective tissue, the muscle fibres in the media being de- 
generated or destroyed. Calcareous deposits may render the 
artery of bony hardness. 

Sequelae. — The weakened vessel wall is predisposed to dilata- 
tion (aneurism of aorta ; miliary aneurisms of cerebral arteries) . 
The thickened walls offer resistance to the blood current, thus 
increasing the pressure and inducing hypertrophy of the left 
ventricle. The reduced lumen of the vessels, by lessening 
the blood supply to various organs, occasions secondary 
sclerotic changes in the latter (interstitial nephritis, fibrous 
myocarditis, hepatic cirrhosis, pulmonary emphysema, etc.). 

Symptoms. — Various superficial vessels, especially the tem- 
poral arteries, appear dilated and tortuous; and a similar con- 
dition may be demonstrated in the radials by palpation. Subjec- 
tive symptoms, when they occur, are due to sequential changes 
in the cerebral circulation (vertigo, head-pains, intellectual 
failure, and hemiplegia from embolism, thrombosis, or hemor- 
rhage), in the heart (symptoms and physical signs of hyper- 
trophy or dilatation), in the kidney (evidences of nephritis), 
or in peripheral circulation (dry gangrene). 

Diagnosis. — The association of high arterial tension, hyper- 
trophy of the left ventricle, accentuation of the aortic second 
sound, and thickened arteries affords positive evidence of 
arterio-sclerosis. 

Prognosis. — The condition is irremediable, but the patient 
may nevertheless live to an advanced age. 

Treatment. — Treatment must be directed to the causes, gouty 
or otherwise. The diet should be simple, nourishing, and non- 
stimulating. Active exertion must be avoided, and the hours 



142 DISEASES OF THE CIRCULATORY SYSTEM. 

of sleep prolonged. The skin should be kept active by frequent 
bathing, and constipation must be avoided. The principal 
medicines are aurum, cuprum, plumbum, and the iodides. 
Glonoin 2x, in drop doses, may be used to lessen the high 
arterial tension. Complicating conditions will suggest other 
remedies. 



ANEURISM. 

Etiology. — Dilatation of a portion of an arterial wall may be 
due to: 

1. Arterio-sclerosis, and hence the causes of the latter, not- 
ably gout and syphilis. 

2. Sudden intense strain. Most cases of aneurism originate 
during the period of greatest physical activity, between the 
thirtieth and fiftieth years of life; but it is probable that strain 
is effective only when arterial degeneration pre-exists. 

3. Embolism of a vessel, if complete, may be followed by 
aneurismal dilatation at its proximal side. 

4. Parasites may induce local arterial changes which lead to 
dilatation. 

Pathology. — A fusiform or cylindrical aneurism is simply a dila- 
tation of an artery at some point. A saccular aneurism is due 
to the bulging of a circumscribed portion of an arterial wall as 
the result of disease or injury; in the sac thus formed the 
intima is ruptured, the media atrophied, and the wall consists 
of the adventitia, fibrous tissue, and adherent surrounding 
strictures. It contains laminated clot, which may later be- 
come organized. 



ANEURISM OF THE THORACIC AORTA. 

Aneurism involves the thoracic aorta in 75% of all cases, the 
abdominal aorta and its branches being affected in but 25%. 
Nearly two-thirds of the thoracic cases occur in the ascending 
portion, and most of the others in the arch. 



DISEASES OF THE CIRCULATORY SYSTEM. 143 

Symptoms. — 1. Pain is usually present. It varies, according 
to the site of the aneurism, from vague distress to intense bor- 
ing and gnawing sensations and even anginal attacks. 

2. Pressure symptoms. These may be due to — 

a. Pressure upon the great veins. Sudden compression of 
the vena cava may occasion edema of the head, neck and 
upper extremities, with dyspnea and cyanosis. Gradual com- 
pression is met by the establishment of collateral channels, 
which may appear as tortuous veins on the surface of the 
chest. The jugulars may become distended and are not 
emptied by a deep inspiration, nor do they pulsate, as when 
the distention is due to venous back-pressure. Obstruction of 
one innominate vein may occasion unilateral distention of the 
internal and anterior jugulars, which does not disappear on 
deep inspiration. 

b. Pressure upon the root of the lung. Pressure on one 
bronchus permits the entrance of only a certain amount of air, 
and this may occasion changes in the breath sounds. There 
may be pressure on the pulmonary veins, causing great con- 
gestion of the lungs; on the cilio-spinal branches of the sympa- 
thetic, causing dilatation or contraction of the pupil on the 
corresponding side; or on the left recurrent laryngeal nerve, 
causing paralysis of the left vocal cord (hoarseness). 

c. Pressure on the trachea (dyspnea), esophagus (dys- 
phagia), or thoracic duct may occur. 

Physical Signs. — 1. Pulsation, expansile in character, in an 
abnormal situation (usually above the third rib) can some- 
times be seen and otherwise may be felt. 

2. A characteristic vibratory thrill, and a diastolic shock at 
the end of the pulsation, may be felt. 

3. A traclieal tug may be detected. The examiner, stand- 
ing behind the patient, supports the latter's head against his 
body, and places the tips of his fingers beneath the cricoid, 
putting the trachea gently on the stretch. A short tug, felt 
with each cardiac systole, is an important sign of aneurism or 
dilatation of the aorta. 



144 DISEASES OF THE CIRCULATORY SYSTEM. 

4. Dulness on percussion in a suspected area may be the 
most important early sign of aneurism. 

5. A loud, lozv-pitched aortic second., sound may be heard. 

6. A murmur may or may not be present. 

7. The pulse of one side may be smaller than the other, or 
it may be delayed. 

8. The auscultatory signs of pressure on the root of one 
lung may be discovered. 

Diagnosis. — Aneurism of the ascending arch usually ap- 
proaches or penetrates the chest wall about the second inter- 
space just to the right of the sternum. It may occasion pain, 
dulness, pulsation, and thrill. 

Aneurism of tlie transverse arch is usually recognized only 
by pressure symptoms (cough, hoarseness, tracheal tug, un- 
equal pupils, etc.). 

Aneurism of the descending aorta occasions severe, persist- 
ent pain in the back, and in advanced cases dulness and pulsa- 
tion may be found in the region of the left scapula. 

Aneurism of the abdominal aorta is associated with sharp 
pain in the back, often increased by eating and drinking, and 
various gastro-intestinal symptoms ; the femoral pulse may be 
delayed, and a pulsating, expansile tumor may be discovered. 
This must be distinguished from the pulsating aorta of nervous 
women, which presents neither pressure symptoms nor definite 
tumor. An abdominal tumor may receive pulsation from the 
adjacent aorta, but it is non-expansile, and is accompanied by 
cachectic and other characteristic conditions. 

Prognosis. — The course of aneurism may be prolonged over 
several years, but it ultimately proves fatal, either by rupture 
or gradual circulatory failure. 

Treatment. — This is unsatisfactory. Various mechanical 
measures, such as galvano-puncture or the introduction into 
the sac of foreign substances, such as silver wire, have been 
used in an effort to induce obliteration of the sac by clotting. A 
more popular method is that which places the patient at rest, 



DISEASES OF THE CIRCULATORY SYSTEM. 145 

upon a light, dry diet, and administers potassium iodide, gr. 
x-xx, three times a day for a period of weeks. Good results 
have in a few cases followed the hypodermatic injection at 
weekly intervals of a few c.c. of a solution of gelatin (1-5%) 
in a normal saline solution. These measures are calcu- 
lated to increase the coagulability of the blood and thus 
favor clotting within the sac of the aneurism. 



10 



DISEASES OF THE RESPIRA- 
TORY SYSTEM. 



DISEASES OF THE UPPER RESPIRATORY TRACT. 

Diseases of the upper air passages (nose, throat, and larynx) 
may be indicated by a variety of symptoms. Attention is 
frequently attracted to the nose by discharge, pain, and 
occlusion, and nasal disease is a common cause of frontal 
headache, especially when the frontal sinus is involved. Neu- 
ralgia may be due to disease of the accessory chambers, 
notably the antrum. Epistaxis is often the result of local 
conditions, but its constitutional causes (anemia, arterio- 
sclerosis, etc.) must not be overlooked. Mouth-breathing 
results from occlusion of the nose by hypertrophic catarrh, 
polypi, septal deviations, adenoid vegetations, etc. ; and cer- 
tain reflex neuroses, notably asthma and hay fever, can 
sometimes be traced to disease of the nose. 

In most of these conditions the pharynx is involved. The 
voice may become nasal as the result of paralysis (post-diph- 
theritic) or ulceration (usually syphilitic) of the soft palate, 
or it may be due to total occlusion of the nose by catarrh or 
polypi. 

Disease of the larynx also occasions changes in the voice, 
which may become hoarse, indistinct, or even lost. 

Dyspnea may result from narrowing of the glottis (diph- 
theria, laryngitis, edema, or paralysis); it is inspiratory in 
■character, often accompanied by stridor, and must be distin- 
guished from tracheal stenosis, in which the larynx does not 
move in inspiration and the voice is not hoarse. Laryngeal 
pain is common but without special diagnostic significance. A 



148 DISEASES OF THE RESPIRATORY SYSTEM. 

laryngeal cough is usually loud and barking ("croupy"), and 
expectoration may accompany it. Dysphagia occurs when 
disease of the larynx has involved the epiglottis and posterior 
wall. 



CLINICAL EXAMINATION OF THE UPPER AIR PASSAGES. 

The patient should be seated facing the examiner, with a 
light placed a little to one side of his head and on a level with 
the eye of the examiner. The latter adjusts a head-mirror to 
his forehead and manipulates it until the hole in its centre is 
directly opposite his right eye and the light is directed into 
the patient's nares. 

1. The nose. Lift the tip of the nose with the finger, and 
note if there be any eczematous or ulcerated condition of the 
skin or mucous membrane, any dried secretion or blood, and 
any ulcer or perforation of the septal cartilage. Then gently 
introduce a speculum and separate the blades. As the inferior 
turbinated comes into view, notice whether it is enlarged; and 
if it appears to be, touch it with a probe to determine whether 
it consists of swollen mucous membrane or bone. Depress 
the patient's chin slightly to bring the inferior meatus into 
view, and then have him tilt his head back a little so that the 
middle meatus and middle turbinated can be seen. The 
superior turbinated can rarely be seen, the superior meatus 
never. Inspect the septum, searching for spines, deviations, 
ulcers, or perforations. 

Then select the smallest laryngeal mirror and hold it face 
downwards over the lamp until a cloud passes over its surface, 
and touch it to the cheek or back of the hand to ascertain that 
it is not too hot. Have the patient depress his chin slightly 
and open his mouth, and introduce a tongue-depressor, hold- 
ing it with the left hand. Grasping the mirror, like a pen, in 
the fingers of the right hand, introduce it, face upwards, be- 
hind the soft palate ; and by rotating it a little the posterior 
nares can be seen. With the posterior end of the septum in 
the centre, on either outer wall the middle turbinated appears 



DISEASES OF THE RESPIRATORY SYSTEM. 149 

as a bluish-red swelling, with the superior meatus and superior 
turbinated above it and the middle meatus and inferior turbin- 
ated below. Notice the size of each of these, its color, and 
the presence of mucus or pus. Then turn the mirror to face a 
little more directly upwards and to one side and look for the 
projecting bright red cushion which limits the depression lead- 
ing to the orifice of the eustachian tube. Notice whether 
there is any secretion at the mouth of the latter. Finally, 
turn the mirror upwards and look for adenoid or other tumors 
at the vault of the naso-pharynx. 

2. The Pharynx. — With the aid of the tongue-depressor those 
portions of the pharynx, soft palate, and fauces not compre- 
hended in the nasal examination should be inspected. Note 
the color ; the yellow tinge of jaundice or the patchy redness 
of measles may be discovered. Notice the presence of ulcers 
or mucous patches. Note whether the tonsils are enlarged, 
and whether they exhibit any grayish patches ; if they do, try 
to wipe them off and see whether a healthy or a raw surface 
(diphtheria) is left. Examine the pharynx. Generally a 
number of swellings like sago-grains can be seen ; if they are 
much increased there is granular pharyngitis. Note if there 
is any ulceration, any excess of mucus, or if there is any 
bulging (retro-pharyngeal abscess). 

3. The Larynx. — Have the patient put out his tongue and 
grasp it between the folds of a clean, dry napkin, and with- 
draw it sufficiently to expose the vault of the pharynx. Intro- 
duce the mirror slowly, without touching tongue or palate, 
until, as the soft palate rises during inspiration, the back of 
the mirror can be placed at the vault of the pharynx. Then 
raise or lower the handle of the mirror until the back of the 
epiglottis comes into view. Tell the patient to say ''a" and, 
as a rule, the vocal cords can be seen. Notice the color of the 
cords and mucous membrane, the presence of any swelling or 
ulceration, and the position and mobility of the vocal cords. 

It is well to caution the patient in advance to breathe regu- 
larly through his nose ; this engages his attention and often 
prevents gagging. In many cases the application of cocain 



150 DISEASES OF THE RESPIRATORY SYSTEM. 

(5%) to the pharynx is a necessary preliminary to examina- 
tion ; and at best the latter is often unsatisfactory the first 
time. 



ACUTE RHINITIS. 

(Coryza; Cold in the Head.) 

Etiology. — Acute catarrhal inflammation of the nasal mucous 
membrane may be primary, due to exposure to cold and wet 
or to inhalation of irritants (dust, chemicals), or secondary, a 
symptom of measles, influenza, etc. Depressed nutrition pre- 
disposes to attacks. 

Pathology. — As a result of vasomotor dilatation the mucous 
membrane becomes red, swollen, congested, and covered with 
secretion, and the passages are obstructed. 

Symptoms. — The attack usually begins with sneezing, and 
dryness and obstruction of the nasal passages, the latter often 
compelling the patient to breathe through his mouth. In a 
few hours a watery, sometimes irritating, secretion appears, and 
later this becomes muco-purulent. Mild febrile symptoms ac- 
company the disease. The inflammation may extend to the 
frontal sinus, causing frontal headache, facial pains, etc. ; it 
may occasion conjunctivitis, pharyngitis, laryngitis, bronchitis; 
or by involving the eustachian tube it may cause temporary 
deafness. 

Prognosis. — Recovery within a week or two. 

Treatment. — For the early stage, administer aconite, bella- 
donna, camphor, or gelsemium. When secretion appears, 
cepa, kali bicliromicum, Pulsatilla, or sulphur may be indi- 
cated. If there is much obstruction, ammonium carb., ly co- 
podium, mix vomica, or sticta will be preferable. Sprays of 
albolene or other oils, plain or mentholated, are beneficial. 



DISEASES OF THE RESPIRATORY SYSTEM. 151 

CHRONIC RHINITIS. 

(Chronic Nasal Catarrh.) 

Etiology. — Chronic catarrh of the nasal passages, character- 
ized by a persistent muco-purulent discharge, may be symp- 
tomatic of a variety of conditions, including the following : 

1. A simple chronic catarrh, in which the mucous mem- 
brane remains more or less congested and slight exposure 
excites acute coryza. 

2. Chronic hypertrophic rhinitis, in which there is a spongy 
overgrowth over the middle and inferior turbinated bones. 
The surface is covered with thick, tenacious mucus, and nasal 
spurs and deflections of the septum are common. 

3. Atrophic rhinitis ', in which there is wasting of the tissues 
which often involves the bone, as a result of which the nasal 
chamber is enlarged and contains offensive secretions and 
crusts (ozczna). 

4. Caries and necrosis of the nasal bones is also accom- 
panied by offensive discharge, the nature of the lesion being 
recognized through the use of the probe to manipulate the 
sequestrum. 

5. Ulcerations in the nose are discovered only by exami- 
nation. They may sometimes be syphilitic, rarely tuber- 
cular. 

6. Foreign bodies in the nose occasion chronic catarrhal 
symptoms. 

Diagnosis. — The recognition and distinction of these lesions 
is possible only by means of careful anterior and posterior 
rhinoscopy. 

Prognosis. — Simple catarrh is readily curable, and hyper- 
trophic rhinitis becomes so under proper treatment. Atrophic 
rhinitis, and caries and necrosis, can be mitigated but not 
cured. The prognosis of an ulceration is governed by its 
cause. The catarrhal condition due to a foreign body is 
usually controlled by the removal of the latter. 



152 DISEASES OF THE RESPIRATORY SYSTEM. 

Treatment. — 1. Cleanse and keep clean the nasal cavities. 
Spray the passages with Dobell's or some similar solution, by 
means of a nasal douche or an atomizer, until they are cleared 
of mucus and dust. Follow this with a spray of albolene, 
plain or mentholated. 

2. Remove the hypertrophied tissue. For this purpose the 
snare, acids, or the galvano-cautery may be used. 

3. Improve the general health of the patient. General 
diathetic states, such as gout or syphilis, should be discovered 
and treated; and the patient's hygiene, diet, etc., should receive 
careful attention. 

4. Medicines. In simple muco-purulent catarrhs, Hydrastis, 
kali bichromicum, Pulsatilla, and sulphur are valuable reme- 
dies. Iodide of arsenic is suited to cachectic patients, aurum 
and nitric acid to cases with offensive discharges, and many of 
the constitutional remedies may be indicated by associated 
conditions. 



HAY FEVER. 

(Autumnal Catarrh; Rose Cold; etc.) 

Etiology — The exciting cause appears to be the inhalation of 
some irritating substance, such as the pollen of plants. The 
predisposing factors are the spring or autumn season, pre- 
existing chronic rhinitis, heredity, a neurotic constitution, and 
the uric acid diathesis. 

Symptoms. — The disease is a peculiar catarrhal affection 
which recurs with marked periodicity once each year. The 
onset occurs suddenly at the appointed time, the attack be- 
ginning with sneezing, coryza, occlusion of the nostrils, burn- 
ing and pricking sensations, and profuse watery discharges. 
Headache is common, conjunctivitis may be present, and 
bronchitis or asthma may develop at any time. As the attack 
progresses the discharge becomes thicker and muco-purulent. 

Prognosis. — For relief, good ; for permanent cure, doubtful. 



DISEASES OF THE RESPIRATORY SYSTEM. 153 

Treatment. — The attack promptly disappears upon removal 
to certain districts, notably the Adirondacks and White Moun- 
tains. Temporary relief may be obtained by cleansing the 
nasal passages with alkaline sprays and applying hydrogen 
dioxid or solutions of supra-renal extract to the mucous 
membrane. Permanent cure may be secured in cases due to 
chronic catarrhs or gout by persistent treatment of the latter 
conditions. Arsenic is the most successful medicine; it may 
also be used as potassium arsenitc, quinine arsenite, cuprum 
arsenite, or arsenic iodide. Kali iod., sticta, euphrasia and 
many other remedies may be successful when indicated. 

ACUTE CATARRHAL LARYNGITIS. 

Etiology. — Acute inflammation of the mucous membrane of 
the larynx may be caused by exposure to cold and wet, the 
inhalation of irritants (dust arid chemicals), the excessive use 
of the voice, and traumatism by foreign bodies, corrosive 
poisons, etc. Heredity, bad hygiene, and diathetic states pre- 
dispose to it. 

Symptoms. — The throat becomes dry and the voice husky or 
lost. Tickling in the throat produces a dry, teasing cough, 
which is later accompanied by viscid expectoration, and there 
may be some fever and pain in the tJiroat, the latter being 
more marked on speaking or swallowing. In children spasm 
of the glottis is added, and produces stridulous breathing and 
croupy cough {spasmodic, catarrhal, or false croup). Exami- 
nation reveals redness of the mucous membrane, involving 
the vocal cords. 

Diagnosis. — By symptoms and examination. 

Prognosis. — In adults the prognosis is favorable unless edema 
supervenes. In children the danger to life, in spite of the 
alarming character of the symptoms, is usually slight. 

Treatment. — Children subject to attacks of acute laryngitis 
should spend their lives out of doors, their hygiene and consti- 
tutional conditions being carefully investigated in the mean- 



154 DISEASES OF THE RESPIRATORY SYSTEM. 

time. During an attack the patient should be placed in a 
room the atmosphere of which is kept at an even temperature 
(70°) and moist with steam. Aconite should be given early, 
and as the symptoms become more severe iodine, bromine, 
or spongia may be prescribed. Belladonna, hepar, kali tick., 
or phosphorus is less often required. Rarely intubation or 
tracheotomy may be necessary. 



CHRONIC CATARRHAL LARYNGITIS. 

Etiology.— This is due to the same causes as the acute form. 

Symptoms.— Persistent hoarseness and cough, viscid expec- 
toration, and tickling in the throat. Examination reveals 
congestion of the laryngeal mucous membrane, with small 
granulations, and reddening of the vocal bands. 

Prognosis. — Guardedly favorable under proper treatment. 

Treatment. — Complete rest of the voice and the avoidance of 
exposure are necessary. Spray the naso-pharynx and larynx 
freely with alkaline solutions, following that with sprays or 
direct applications of iodine or astringents. Causticum, hepar, 
kali Inch., and phosphorus are the more important medicines. 



EDEMATOUS LARYNGITIS. 

Etiology. — Edema glottidis may be — 

1. Primary, originating in the larynx (rare). 

2. Contiguous, spreading from adjacent tissue (pharynx). 

3. Consecutive, following perichondritis or other disease of 
the larynx. 

4. Symptomatic of certain diseases, especially the acute 
infections. 

Symptoms. — A feeling of obstruction in the larynx is quickly 
followed by dyspnea, stridulous breathing, and sometimes 
suffocation. The swelling is easily seen with the laryngo- 
scope, often without it. 



DISEASES OF THE RESPIRATORY SYSTEM. 155 

Treatment. — Place the patient at rest and let him hold in the 
mouth or swallow small pieces of ice. If the symptoms are 
threatening, scarification of the laryngeal tissue, intubation, or 
tracheotomy is advisable. Apis, arsenic, iodine, lacliesis, and 
sanguinaria are the remedies usually recommended. 



TUBERCULAR LARYNGITIS. 

Etiology. — As a rule this is secondary to pulmonary tuber- 
culosis ; rarely it is primary. 

Symptoms. — The early symptoms are identical with those of 
simple catarrhal laryngitis, including hoarseness and aphonia. 
Later painful deglutition is complained of, and this, together 
with the obstinacy of the disease, indicates its true nature. 
Before that time, however, examination should have been 
made. It reveals either pearly granulations (miliary tuber- 
cles) or small, shallow ulcers with gray bases on the pale 
mucous membrane. 

Treatment. — In the hands of a skillful laryngologist applica- 
tions of lactic acid may be made to the ulcers, or iodoform 
may be dusted into the larynx. In many cases it is necessary 
to apply cocain to the larynx just before meals in order to 
overcome the painful deglutition. The general treatment of 
tuberculosis must be carried out at the same time. 



SYPHILITIC LARYNGITIS. 

Symptoms. — In the victim of syphilis, hoarseness, cough and 
difficult deglutition should insure examination of the larynx. 
This may reveal an apparently simple laryngitis, or mucous 
patches, ulcers, and even necrosis of the cartilages. 

Treatment. — Local cleansing with sprays, applications of 
silver nitrate, and active mercurial medication are advisable. 



156 DISEASES OF THE RESPIRATORY SYSTEM. 



DISEASES OF THE LOWER RESPIRATORY TRACT. 

As a rule attention is attracted to disease of the respiratory 
apparatus (lungs, bronchial tubes, or pleura?) by symptoms 
directly referable to those organs, e. g., chest pain, cough, ex- 
pectoration of mucus or blood, dyspnea, and changes in the 
voice. It must not be forgotten, however, that serious disease 
may attack the organs of respiration without causing local 
symptoms, the patient complaining only of weakness, loss of 
appetite and of flesh, and perhaps feverishness. Because 
of the insidious nature and vague symptoms of certain dis- 
eases, particularly those of tuberculous origin, it is customary 
to include the respiratory organs in every systematic exam- 
ination. 

Interrogation of the patient. — Should the symptoms elicited by 
general interrogation point to disease of the bronchi, lungs, or 
pleurae, the examiner should inquire particularly regarding : 

1. A family history of bronchitis, asthma, phthisis, or 
scrofula. 

2. The patient's occupation : is he exposed to irritating fumes 
or dust ? 

3. Symptoms. Has he ever had enlarged glands in the neck ? 
Does he sweat at night ? Is he losing weight ? 

Cough : its character and frequency ; when is it worst ? 
Does it cause any pain? Does it ever cause him to vomit? 

Expectoration : its amount and character. Is it yellow or 
not ? Does it ever contain blood ? If so, is it only after severe 
coughing ? Is the blood dark, or frothy and bright ? 

Chest pain : is it worse on taking a full breath ? Is it con- 
stant ? What is its exact location? 

Dyspnea : when does it occur? If it is paroxysmal, let him 
describe an attack. 

Having satisfied himself as to these details, the examiner 
should proceed to the physical examination of the patient. 



DISEASES OF THE RESPIRATORY SYSTEM. 157 



PHYSICAL EXAMINATION OF THE RESPIRATORY ORGANS. 

Place the patient, stripped to the waist, in a good light. It 
is well to inspect the chest with the light striking it obliquely 
as well as directly. By inspection the examiner determines: 

1. The size, form and nutrition of the chest. 

A. Is the chest healthy? (symmetrical, well-nourished, 
etc.). 

B. Is it symmetrical but suggesting proclivity to dis- 
ease ? e. g. , 

A flat chest or " paralytic thorax," i. e., anteropos- 
terior flattening. This is not necessarily phthisical. 
There may be emaciation of the chest wall, indicat- 
ing nutritional failure. 

C. Is it symmetrical but suggesting past disease? e. g., 

the rachitic chest. There may be projection of 
the sternum ("pigeon-breast"); depression of the 
root of the sternum ("funnel-breast"); or the 
"rachitic rosary" (a line of eminences along the 
chondro-costal articulations, more often felt than 
seen). 

D. Is it symmetrical but suggesting present disease? e. g., 

the "barrel-chest" (increased antero-posterior di- 
ameter) of emphysema. Or 
Bilateral retraction of chest walls, i. e. , an extremely 
flat chest. 

E. Are there local changes? For example, 

Deformities. Spinal curvature may be detected by 
marking, if necessary, the position of the spinous 
processes. Such curvature may give rise to con- 
siderable displacement of the thoracic organs and 
so render useless the usual landmarks. Pott's dis- 
ease may be detected, often better by touch than 
by inspection; in its early stages it gives rise to 
muscular rigidity, which must not be confounded 



158 DISEASES OF THE RESPIRATORY SYSTEM. 

with abnormal rigidity of the spinal column itself, 
which persists when the patient bends; the latter 
is due to spondylitis deformans. 

Unilateral flattening may be present as the result of 
chronic phthisis, pulmonary fibrosis, or pleuritic 
adhesions. 

Unilateral prominence may suggest pneumothorax, 
pleural effusion, or possibly emphysema. 

Local bulging may be due to aneurism of the aortic 
arch, tumor (lipoma, gumma, sarcoma) of the chest 
wall or viscera, ''cold abscess" (tubercular) of rib 
or sternum, or empyema perforating the thoracic 
wall. In children, in whom the bony framework is 
soft, precordial bulging may indicate an enlarged 
heart or pericardial effusion. 

Pallor, cyanosis, edema, jaundice, scars, and eruptions, 
if present, should be noted and may lead to a correct 
diagnosis. 

Enlarged glands in the neck or axillae may suggest 
tuberculosis, syphilis, or malignant disease. 
2. Changes in Respiratory Movement. 

A. Normal rate, rhythm, and type. 

B. Abnormal degree of expansion. 

a. Diminished expansion of one side. 

If the chest is distended it may be due to pneu- 
mothorax, pleuritic effusion, or tumor. 

If retracted it is apt to be due to phthisis, pleuri- 
tic adhesions, occlusion of a bronchus by an 
aneurism, etc. 

Restriction of motion of one side of the chest 
may also be due to pressure from enlarged 
viscera or tumors below the diaphragm. 

b. Increased expansion of one side of the chest is 
usually compensatory to interference with respira- 
tion on the other side. 



DISEASES OF THE RESPIRATORY SYSTEM. 159 

C. Dyspnea (difficult breathing) is usually rapid as well 
as labored, and is often accompanied by cyanosis. It 
may be inspiratory, as when the larynx is obstructed 
(croup, foreign body), or expiratory, due to difficulty 
in emptying the chest (asthma, emphysema). 

Simple rapidity of respiration, not dyspnea, is a common 
result of muscular exertion, neurotic disturbances, heart 
and lung disease; and it usually accompanies fever. 

3. Changes in Respiratory Rhythm occur in asthma, where in- 
spiration is a short gasp and expiration a long wheeze; 
and in emphysema, where, however, less dyspnea is 
present. 

In Cheyne-Stokes respiration, periods of apnea (no respira- 
tion) are followed by respirations which are first short 
and shallow, but increase gradually until they are rapid and 
deep, and then as gradually die away until the patient is 
apneic again. This respiratory anomaly occurs in con- 
nection with severe heart, kidney, or brain diseases and is 
of grave significance. 

Restrained breathing, the patient '"catching" his breath, is 
common in pleurisy. 

Shallow and irregular breathing occurs in connection with 
profound unconsciousness from any cause (apoplexy, 
uremia, poisoning). 

Stridulous breatJiing, "crowing," is the result of obstruction 
at the glottis ; it occurs in laryngismus stridulus, whoop- 
ing cough, and larygeal or tracheal obstruction by a 
foreign body. 

4. Changes in the Diaphragmatic Movements may be observed by 
Litten's method. The patient lies on his back with his 
chest bared and his feet pointing directly to the only 
window through which light is permitted to enter. As 
the patient takes a full breath, the observer, standing at 
his side, can see a narrow shadow which moves down 
along the axilla from the seventh to the tenth rib. Dur- 
ing expiration the shadow, less easily seen, rises again to 



160 DISEASES OF THE RESPIRATORY SYSTEM. 

its starting point. The phenomenon represents the excur- 
sion of the diaphragm during respiration. It is absent in 
pneumonia of the lower lobe, pleuritic effusion, or exten- 
sive adhesions. Fluid or solid tumors below the dia- 
phragm, unless very large, do not abolish it. Hence this 
procedure may be of great value in distinguishing an en- 
larged liver or a subphrenic abscess from fluid in the right 
pleural cavity. 
Palpation, usually practiced in connection with inspection, 
determines— 

1. The form of the chest, confirming or modifying the results 
of inspection. 

2. Vibrations of the chest wall. 

A. Vocal or tactile fremitus, the sense of vibration com- 
municated to the hand laid flat upon the chest while the 
patient speaks (usually counting "one, two, three" or 
"ninety-nine" repeatedly), varies greatly in different 
parts of the chest. Allowance being made for these 
normal disparities, fremitus may be— 

a. Diminished or absent, when the lung is pushed 
away from the chest wall by air or fluid in the 
pleural sac. 

b. Increased when the lung is solidified in pneumonia 
or phthisis. 

B. Pleural friction, the rubbing together of the rough- 
ened surfaces in dry pleuris} 7 , may be felt as well as 
heard. 

C. Rales, coarse and dry in character, sometimes com- 
municate a peculiar sensation to the palpating hand. 

3. Tenderness of the thorax may be found in intercostal neu- 
ralgia, in which case it corresponds to the points of exit of 
the intercostal nerves; and it occurs also in case of 
necrosis of a rib, in dry pleurisy, and occasionally in 
phthisis. 

4. Fluctuation or elasticity of any tumor or prominence in the 



DISEASES OF THE RESPIRATORY SYSTEM. 161 

chest wall will convey important information as to its 

character. 
5. The skin temperature; e. g. y the hot, dry skin of fever or 

the cold, clammy skin of circulatory failure, may be 

detected by the palpating hands and affords information 

of diagnostic importance. 
Percussion has for its object the determination of two 
things, viz., 

1. The boundaries of the lungs (topographical percussion). 

2. The resonance of the lungs, including 

A. Variations normal to various parts of the chest. 

B. Variations of resonance abnormal va character. 

a. Quantitative. Increase (hyper-resonance) indi- 
cates emphysema, cavity, etc. 

Decrease (varying in degree from slight impair- 
ment to absolute dulness) indicates thickening 
of chest wall, pleuritic effusion, or solidification 
of lung tissue. 

b. Qualitative. Pitch may be low, medium or high; 
a clear sound of heightened pitch indicates airless 
structure (consolidation, effusion) behind air-con- 
taining structure. 

Cracked-pot resonance, a peculiar "chinking" sound 
produced over a pulmonary cavity or an open pneu- 
mothorax from which the air is suddenly and f orcibly 
expelled by the percussion stroke, is best heard by 
having the patient hold the chest piece of the 
stethoscope in front of his open mouth, leaving the 
examiner's hands free to percuss the chest. This 
sound may be obtained over the chest of any 
healthy infant, especially when crying. 
Amphoric resonance, metallic and echoing in charac- 
ter, may be imitated by percussing the cheek dis- 
tended with air. It is sometimes obtained in pneu- 
mothorax and in phthisical excavation. 
11 



162 DISEASES OF THE RESPIRATORY SYSTEM, 

Auscultation determines : 
• 1. The character of the respiratory sounds. 

A. Vesicular breathing (breezy in character) is heard 
normally over lung tissue. Its intensity may be — 

a. exaggerated in children, 
over thin chest walls. 

after exertion leading to deep forcible breathing, 
over one lung (compensatory) when the other is 

out of use (e. g., as the result of solidification or 

compression by pleural effusion). 

b. diminislied, as a result of — 

the presence of air, solid, or fluid in the pleural 
cavity. 

emphysema, with feeble chest movement. 

bronchitis or edema, lessening the inflow of air. 

pain in the thorax, because of which the patient re- 
strains the chest movements. 

occlusion of the upper air passages (bilateral dimi- 
nution if the glottis is occluded, unilateral if a 
bronchus) 

paralysis of the muscles of respiration. 

B. Bronchial breathing, normally heard over the trachea 
and primary bronchi, is pathologic if heard elsewhere 
and indicates solidification of that part of the lung 
(phthisis, pneumonia, etc.), ox distant bronchial breath- 
ing may be heard over a pleural effusion. 

C. Broncho-vesicular breathing, intermediate in type be- 
tween the bronchial and the vesicular, is heard normally 
near, not over, the trachea, and over the larger bronchi 
at those portions of the chest where they are within 
auscultatory distance but separated from the chest wall 
by a small amount of lung tissue. In the healthy chest 
a broncho-vesicular note is heard over the lower part of 
the manubrium, over the inter-scapular regions at the 



DISEASES OF THE RESPIRATORY SYSTEM. 163 

level of the third dorsal vertebra, and over the apex of 
the right lung. It may be heard elsewhere when disease 
has produced moderate solidification of the lung. 
D. Amphoric breathing, comparable to the hollow, empty 
sound produced by blowing across the top of a bottle, 
is occasionally heard over a large empty cavity within 
the chest or over an open pneumothorax. 
Adventitious Sounds. 

A. Rales, produced by the passage of air through bronchi 
which contain mucus or pus, or which are narrowed by 
swollen walls, may be — 

Moist or bubbling in character {crepitations), and 
coarse {large "mucous" rales), medium, or fine 
{subcrepitant), according to the size of the tube in 
which they are produced; they indicate the pres- 
ence of fluid. 

Dry or crackling (rhouchi), without the bubbling 
character, because the secretion is thick and tena- 
cious. They are described as large (low-pitched, 
sonorous), medium, or fine (small, sibilant rales). 
The finest of all are the crepitant rales, which 
resemble the sound heard on rubbing a lock of hair 
between the finger close to the ear, and are present 
early in pneumonia and more rarely in phthisis, 
edema, etc. 

The groaning, shrieking, and whistling sounds caused 
by the passage of air through tubes narrowed by 
swollen membrane, are also described as musical 
rales. 

B. Pleural friction sounds, rubbing and creaking in char- 
acter, are heard close to the ear, becoming louder if the 
pressure of the stethoscope is increased, and, unlike 
rales, are not influenced by coughing. They suggest 
the roughness of the inflamed pleural surfaces. 

C. Splashing sounds, heard if the ear is held against the 
chest and the patient shaken firmly, indicate the pres- 



164 DISEASES OF THE RESPIRATORS SYSTEM. ' 

ence of both air and fluid in a cavity (pyopneumo- 
thorax, etc). 
D. Metallic tinkling, the sound of a drop of liquid falling 
into fluid at the bottom of a cavity, occurs occasionally 
in pneumo thorax and less often in large pulmonary 
cavities. 
3. Vocal Resonance. 

A. The whispered voice, the patient whispering "one, 
two, three" or "ninety-nine," is heard normally only 
over the trachea and primary bronchi. When audible 
elsewhere it indicates solidification or excavation of the 
lung. 

B. The spoken voice conveys less valuable information 
than the whisper ; it corresponds closely to tactile 
fremitus in its modification by tissue changes. An in- 
crease of vocal resonance is known as bronchophony, 
and the transmission of distinct words rather than con- 
fused sound, is called pectoriloquy. It is discovered 
more often in connection with the consolidation of 
pneumonia than that of phthisis ; it may occur also in 
cases of pneumothorax and pulmonary excavation. 
Egophony, a nasal or squeaky quality of the vocal 
resonance, may be heard in connection with pleural 
effusions and occasionally over consolidated lung. 

BRONCHITIS. 

Bronchitis is a catarrhal inflammation of the bronchial 
tubes, of which the chief symptoms are cough, expectoration, 
and dyspnea. Clinically we distinguish : 

1. Acute bronchitis of the larger tubes (simple bronchitis). 

2. Acute bronchitis of the smaller tubes (capillary bron- 
chitis). 

3. Chronic bronchitis. 

4. Plastic bronchitis (acute and chronic). 



DISEASES OF THE RESPIRATORY SYSTEM. 165 

ACUTE SIMPLE BRONCHITIS. 

Etiology. — The exciting causes of acute bronchitis include — 

1. Chill from exposure to cold and damp. 

2. Infectious diseases (measles, typhoid, etc.). 
The predisposing causes include — 

1. Impurity of the air (deficient ventilation, fog, dust). 

2. Obstruction to the circulation of blood through the lungs 
(chronic valvular disease, emphysema). 

3. Toxemic irritation (gout, B right's disease). 

4. Personal susceptibility (heredity, debility, etc.). 

Pathology. — A bilateral catarrh of the larger tubes, usually in- 
volving the trachea, is present. The mucous membrane is con- 
gested, and there is an increased secretion of mucus mixed 
with desquamated epithelium and leucocytes. 

Symptoms. — The attack may begin as an ordinary catarrh of the 
nose and throat, thence extending down to the bronchi ; or a 
chill may be followed immediately by the typical symptoms. 
These are: 

1. Cough, dry in the early stages and later accompanied by 
free muco-purulent expectoration. 

2. Pain, soreness, or rawness under the sternum ; when 
secretion is established, this is relieved. 

3. Moderate fever (99°-102°) and the usual mild febrile 
symptoms (headache, coated tongue, etc.). 

Physical Signs. — These are often absent. Rales (early, dry ; 
later, moist) may be present. 

Diagnosis. — Influenza is distinguished by its high fever, in- 
tense pains, and great prostration. 

Tuberculosis may present only catarrhal symptoms; if the 
physical signs are limited to one upper lobe or both apices, 
search should be made for the tubercle bacillus. 

The onset of acute infections, such as measles or whooping 



166 DISEASES OF THE RESPIRATORY SYSTEM. 

cough, may be marked by bronchitis, but the later develop- 
ment of typical symptoms and signs will correct the diagnosis. 

Congestion of the hing secondary to mitral disease may be 
deceptive occasionally, owing to the disappearance of the 
murmur; but careful physical investigation of the heart, 
together with the probable reappearance of the murmur as 
the result of rest and treatment, will establish the diagnosis. 

Prognosis. — Good, except at the extremes of life, when capil- 
lary bronchitis or broncho-pneumonia may develop. 

Treatment. — An attack may be aborted at the onset by the 
use of a hot foot or general bath, followed by rest in bed and 
the administration of aconite or gelsemium. 

During the dry stage, with painful cough and scanty expec- 
toration, such remedies as ferrum phos., bryonia, or squills 
are indicated. Hyperesthesia of the larynx, with tickling 
cough, suggests hyoscyamus ; while sensitiveness to external 
pressure, which excites cough, indicates the need of rumex, 
sticta, or lachesis. Ipecac and apomorphia aid in promoting 
secretion; and the appearance of free expectoration calls for 
antim. iod. or kali bich. Cyanotic symptoms may demand 
tartar emetic, or antim. arsen. Co-existing laryngitis may call 
for such remedies as phospliorus, spongia, belladonna, or hepar. 
In old people difficulty in expectoration is relieved by senega 
or amnion, carb. Protracted sub-acute cases may require 
pulsat., sulphur, or stannum. 

The dry cough of the early stage is often greatly relieved by 
the inhalation of steam or of nebulized oils. 



CAPILLARY BRONCHITIS.. 

(Suffocative Catarrh.) 

Etiology. — The causes are identical with those of milder 
bronchitis, the more severe development being due to weaker 
individual resistance (infancy and old age). 

Pathology. — Either by extension from the larger tubes, or 



DISEASES OF THE RESPIRATORY SYSTEM. 167 

primarily, the mucous membrane of the finer tubes becomes 
inflamed, swollen, and occluded with tenacious mucus. Ex- 
tension of the disease to the alveoli (broncho-pneumonia) or 
collapse of the lung areas beyond the bronchial occlusion 
usually follows. 

Symptoms. — 1. Cough with little expectoration. 

2. Rapid respirations (68-80 per minute). 

3. High fever (104°-105°) with restlessness and delirium. 

4. Dyspnea and cyanosis, with weak, rapid pulse (120 or 
more) and evidence of failing heart. 

Physical Signs. — 1. Distention of the upper part of chest with 
recession of the lower, due to respiratory stenosis. 

2. Fine "hissing" rales posteriorly on both sides. 

3. The ordinary sounds of bronchitis (dry rales) over the 
upper anterior part of chest. 

4. Dulness over the areas of collapse or of broncho-pneu- 
monia. 

Diagnosis. — Pneumonia has a sudden onset, a severe rigor 
being followed with high temperature and pain in the side, 
but there is less subjective dyspnea and usually the physical 
evidences of pre-existing bronchitis are lacking. 

Miliary tuberculosis has an insidious onset, with pallor, 
wasting, etc. 

Prognosis. — This is very grave at the extremes of life, death 
from heart failure or asphyxia frequently occurring within a 
few days. In vigorous adults the disease is less fatal. 

Treatment. — Place the patient at absolute rest in a room 
heated to 70° or more and keep the air moistened with steam. 
Stimulation of the respiratory muscles by gentle friction is 
helpful. In addition to the other remedies useful in simple 
bronchitis, grave symptoms, such as dyspnea or cyanosis, call 
for the administration of tartar emetic, antim. arseu. y or 
apomorphia. Evidence of impending heart failure demands 
alcoholic or other stimulants. 



168 DISEASES OF THE RESPIRATORY SYSTEM. 



CHRONIC BRONCHITIS. 

Etiology. — Chronic bronchial catarrh may be : 

1. A sequel of repeated acute attacks, and consequently due 
to the exciting causes of the latter (cold, exposure, etc.). 

2. Secondary to local lung lesions (emphysema, phthisis, 
and pulmonary stasis from mitral disease). 

3. Associated with general sclerotic changes (gout, chronic 
nephritis, senile degeneration). 

Pathology* — The mucous membrane is smooth, congested, of 
greyish hue, and thickened with a connective tissue overgrowth. 
Irregular dilatation of the tubes (bronchiectasis), emphy- 
sema, and dilatation of the right heart often ensue. 

Symptoms.— 1. Cough, not necessarily continuous, but tend- 
ing to become persistent (e. g., the chronic "winter cough" of 
elderly people). 

2. Expectoration, which may be scanty {dry catarrh), severe 
paroxysms of cough dislodging little sputum ; or profuse and 
muco-purulent, and sometimes extremely copious {bron- 
chorrJiea). 

3. Dyspnea, especially on exertion, in cases of long standing 
in which emphysema has developed. 

Physical Signs. — Moist rales, often associated with feeble 
breath sounds and other evidences of emphysema. 

Diagnosis. — Tuberculosis must be excluded by the absence of 
evidences of consolidation and of the tubercle bacillus in the 
sputum. 

Prognosis. — Under favorable circumstances the bronchial 
catarrh can be controlled ; but emphysema cannot be re- 
moved, and associated changes in the heart or kidneys will 
render the prognosis much more grave. 

Treatment. — 1. Attention to the cause (gout, heart or kidney 
disease). 

2. Hygienic : nutritious diet, warm clothing, bathing, etc. 



DISEASES OF THE RESPIRATORY SYSTEM. 169 

3. Climatic : if possible change of residence to a climate 
affording even temperature, moderate warmth and dry atmo- 
sphere. 

4. Medicinal. Dry catarrhs are benefited by such remedies 
as bellad., iodine, rumex, or spongia. With free muco-puru- 
lent expectoration the list of useful medicines includes arsen. 
iod., antim. iod., stannum, stanmun iod., kali biclirom. or carb., 
lycopodium, pidsatilla, and sulphur . Difficult expectoration in 
the aged suggests the use of amnion, carb. or senega. Asso- 
ciated changes in the heart or kidneys will furnish other thera- 
putic indications. 

Inhalations of creosote or terebene are of great value in 
cases attended with free muco-purulent expectoration. 



PLASTIC BRONCHITIS. 

(Croupous, Membranous or Fibrinous Bronchitis.) 

This is a rare disease of uncertion causation in which the 
ordinary symptoms of bronchitis are accompanied from time 
to time with the expectoration of fibrinous casts of the tubes, 
often with a small quantity of blood. The liability to recur- 
rence of these acute attacks renders the disease essentially 
chronic. 

The prognosis for life is good ; for recovery bad, often un- 
favorable. The treatment is that of chronic bronchitis. 

BRONCHIECTASIS. 

(Dilatation of the Bronchial Tubes.) 

Etiology. — Dilatation of the bronchial tubes is invariably sec- 
ondary to lesions weakening the bronchial wall and permitting 
its dilatation under coughing pressure ; these include: 

1. Congenital weakness of the bronchial wall (rare). 

2. Inflammations leading to atrophy of the bronchial wall 
(chronic bronchitis). 



170 DISEASES OF THE RESPIRATORY SYSTEM. 

3. Obstruction by foreign bodies or tumors, the tube beyond 
the point of obstruction becoming dilated. 

4. Traction on the tube by the adjacent lung (pulmonary 
collapse, pneumonia, fibrosis, etc.). 

Pathology. — Cylindrical dilatation or sacculation of the tube, 
occurs, and it is usually associated with local inflammatory or 
ulcerative changes in the mucous membrane. Fetid secretion 
accumulates in the sac thus formed, and ultimately occasions 
characteristic symptoms. 

Symptoms. — Moderate dilatation of a bronchial tube causes 
no symptoms, but the presence of a sacculation gives rise to 
paroxysms of cough attended by the expectoration of large 
quantities of purulent, often fetid, secretion. This results 
from the sac, itself insensitive, becoming gradually filled up 
and overflowing; with the cough thus excited, the collection 
is emptied out and for some hours, while the sac is again fill- 
ing, the patient may be free from cough. 

Physical Signs. — As a rule, these are limited to indications of 
the associated conditions; but in well-marked cases the saccu- 
lation affords the physical signs of a cavity (tympany, me- 
phoric breathing, gurgling rales, bronchophony). These are 
discoverable only when the sac is quite empty. Its location 
at the base of the lungs aids in distinguishing the latter from a 
tubercular excavation. 

Diagnosis. — Tuberculosis is distinguished by the presence of 
tubercle bacilli and elastic tissue in the sputum; usually there 
is fever and cachexia. 

A circumscribed empyema rupturing into the lung presents 
similar physical signs, but its sudden development, with a his- 
tory of previous pleurisy, establishes the diagnosis. 

Prognosis. — The prognosis as to life is governed by the asso- 
ciated conditions. Bronchiectasis itself is chronic and only 
palliation is possible. 

Treatment should be directed to the causative condition. 
Emptying of the sac is aided by gravity if the patient "coughs 
down hill," i. e. y lies on a couch with head and shoulders 



DISEASES OF THE RESPIRATORY SYSTEM. 171 

hanging down toward the floor. Antiseptic inhalations or 
sprays (creosote, carbolic acid), or intra-tracheal injections of 
mentholated oil may lessen the fetid expectoration. The 
drainage of the sac by surgical means may be considered. 



ASTHMA. 

(Spasmodic, Bronchial, or Essential Asthma.) 

Symptomatic dyspnea of varying origin has been mis-called 
asthma, with a prefix (cardiac, renal) to denote its source. 
The term should, however, be restricted to the neurotic form. 

Etiology. —The attack is due to spasmodic contraction of the 
bronchioles, of reflex origin, and its causes may be — 

1. Neurotic temperament and heredity. 

2. The gouty diathesis. 

3. Diseases of the respiratory tract (nasopharyngeal ca- 
tarrh, adenoids, polypi; enlarged tonsils; bronchitis). 

4. Various irritants (certain climates, odors, dust, etc.). 
Symptoms.— The typical attack is a paroxysmal dyspnea 

usually occurring at night. After few, if any, prodromes, 
the patient is suddenly seized with a sense of oppression, and 
this rapidly develops into distressing difficulty in breathing. 
Expiration is labored and becomes a prolonged wheeze; the 
chest is distended and the auxiliary muscles of respiration are 
called into use without effect. At the height of the attack the 
face become pale and perhaps cyanosed, and the body is cold 
and covered with sweat; the patient's distress is frightful. At 
first there is a tight cough without any rales, but later moist 
rales are heard, and small, tough masses aperies) of sputum are 
expectorated. These balls can be unrolled in water and appear 
to be spirals of mucus moulded in the finer tubes (Curschmann's 
spirals); they contain octahedral crystals (Leyden's) identical 
with those found in leukemic blood and in semen. 

After a period of suffering often extending over several 
hours, the breathing becomes easier, the cough lessens, and 



172 DISEASES OF THE RESPIRATORY SYSTEM. 

the patient falls asleep. The attack may recur in a few hours, 
or the patient may remain well for weeks. 

Diagnosis. — Symptomatic dyspnea, due to cardiac or renal dis- 
ease, must be excluded by careful consideration of the history 
and by an examination directed to those organs. 

Laryngeal or tracheal obstruction occasions inspiratory, not 
expiratory, difficulty ; and the chest is diminished in size, not 
distended. 

Prognosis.— A cure is rendered possible by discovery and 
removal of the cause. The disease if uncontrolled tends to 
produce emphysema and dilatation of the right heart ; and 
these conditions, when established, render recovery impossi- 
ble, although life may last for years. 

Treatment. — The paroxysm may be modified by the adminis- 
tration of such remedies as arsenic, grindelia, ipecac, lobelia, 
and nux vomica. If these fail and the attack be extremely 
violent, recourse may be had to inhalations of amyl nitrite or 
to morphia, gr. %, hypodermatically ; but in general these 
palliative measures are distinctly prejudicial to ultimate 
recovery. 

In the intervals between paroxysms careful search must be 
made for the cause. The gouty diathesis if present must be 
overcome, nasal and pharyngeal diseases must be treated, and 
the patient's general hygiene should be supervised is every 
detail. 

The remedies which have proven useful include bryonia and 
ipecac in cases associated with bronchial catarrh ; and cuprum, 
cuprum arsen., chininum sulph., arsen., nux vomica, hydro- 
cyanic acid, and chloride of gold in purely neurotic cases. 
Other remedies may be indicated by associated conditions. 

CONGESTION OF THE LUNGS. 

Etiology. — Hyperemia of the lungs may be — 
1. Active. It occurs as an early stage in the various in- 
flammatory affections of the lungs, or independently as the 



DISEASES OF THE RESPIRATORY SYSTEM. 173 

result of inhaling hot air, irritants, etc. It may occasion 
dyspnea, cough, and expectoration. A diagnosis can be made 
only by exclusion. 

2. Passive, (a) Hypostatic. Feeble heart action, such as 
occurs in the aged or infirm or the victims of long-continued 
fever, together with altered blood states and the force of 
gravity, may lead to congestion of the dependent portions, 
usually the bases, of both lungs. Following this, the air cells 
may collapse and a species of pneumonia develop {hypostatic 
pneumonia). 

(b) Mechanical or obstructive. Any condition, such as 
mitral disease or dilatation of the right ventricle, which 
prevents the return of blood to the left heart, leads to con- 
gestion, followed by connective tissue hyperplasia and 
pigmentation, in the lung (brown induration). The symptoms 
are principally those of the heart lesion; they include cough, 
dyspnea, palpitation, and oppression, and sometimes 
hemoptysis. The discovery of generally distributed fine rales 
indicates the pulmonary condition. 

3. Edema of the lungs represents a further stage of con- 
gestion. Effusion of serous fluid into the air vesicles may 
occur as : 

{a) Collateral edema, a localized process around an inflamed 
area. 

(b) General pulmonary edema, due to 

(1) Weakness of the left heart, the right remaining un- 
impaired. In consequence of this the pressure of the 
blood in the pulmonary circulation becomes increased 
to such an extent that exudation of serum into the air 
vesicles ensues. 

(2) Hydremic conditions associated with impaired nutri- 
tion of the vascular walls, such as are present in cases 
of profound anemia nephritis, septicemia, etc., may 
lean to escape of the serum into the vesicles. This 
often occurs during the death agony. 



174 DISEASES OF THE RESPIRATORY SYSTEM. 

Symptoms. — The onset of pulmonary edema is attended with 
an increased frequency of respiration, dyspnea, and cough ; 
and the latter is accompanied by the expectoration of a 
frothy, watery, and sometimes blood-stained, serum. Fever 
does not occur unless there is an inflammatory condition pres- 
ent elsewhere. The extremities are usually cool, and cyanosis 
may develop. Physical examination reveals incomplete dul- 
ness and crackling and bubbling rales over the areas involved, 
which are usually at the bases of both lungs. 

Treatment. — The treatment of congestion of the lungs, what- 
ever its variety, must be directed to the causal condition. 
In those forms which are associated with heart weakness, and 
especially if pulmonary edema occurs, it may be necessary to 
resort temporarily to such remedies as strychnine, gr. ^— ^V, 
caffein sodio-benzoate, gr. i, or atropine, gr. riii- Edema 
also affords indications for the administration of such medi- 
cines as ammonium carb., arsenic, phosphorus, and tartar 
emetic. 

HEMOPTYSIS. 

Etiology. — Blood may be expectorated as the result of — 

1. Pulmonary lesions. 

(a) Pulmonary congestion in the early stages of pneu- 
monia, or secondary to heart disease, etc. 
(£) Pulmonary embolism. 

(c) Pulmonary tuberculosis. 

(d) Pulmonary gangrene. 

(e) Pulmonary carcinoma. 

2. Bronchial lesions. 

(a) Bronchitis, acute, chronic, or fibrinous. 

(b) Bronchiectasis. 

(c) Ulceration of the bronchial tubes, or of the larynx or 
trachea. 

3. Cardio-vascular lesions, occurring in : 



DISEASES OF THE RESPIRATORY SYSTEM. 175 

Arterio-sclerosis, aneurism, purpura, hemophilia, and cer- 
tain acute infections. 

4. Traumatism. Injuries and contusions of the chest, etc. 

Symptoms and Diagnosis. — As a rule the patient first notices a 
salty taste in the mouth, and this is quickly followed by the 
expectoration of frothy, bright red blood in varying quantities. 
There may be pain in the side, dyspnea, and even syncope. 
Auscultation may reveal moist rales together with evidences of 
the causative disease, but any more extended physical investi- 
gation is inadvisable until after the hemorrhage has ceased. 
It is important to exclude epistaxis, in connection with which 
blood may enter the naso-pharynx and be expectorated ; and 
bleeding from the gums, or from the pharynx. As a rule this 
can be accomplished by simple inspection. In liematemesis 
the blood is dark in color, often clotted or mixed with rem- 
nants of food, and the associated symptoms are referable to the 
stomach. 

Treatment. — Place the patient at rest in a semi-recumbent 
position, let him swallow small bits of ice, and administer such 
remedies as aconite, arnica, erigeron, ergot, ferritin pJios., 
geranium, hamamelis, hydrastinine hydrocJdorate, ipecac, and 
millefolium. In grave cases morphia may be given hypo- 
dermatically. 

EMPHYSEMA. 

Interlobular or Interstitial Emphysema, the condition 
in which air, escaping from ruptured vesicles, collects in the 
interlobular tissue and there appears like rows of beads out- 
lining the lobules, is not recognizable clinically and, more- 
over, possesses nothing in common with vesicular emphysema 
but the name. 

Vesicular emphysema may be local (compensatory) or 
general; and the latter may be hypertrophic, "large-lunged," 
or atrophic, "small-lunged." 

Etiology. — The condition is one of dilatation of the alveoli 



176 DISEASES OF THE RESPIRATORY SYSTEM. 

associated with imperfect contractility of the lung tissue, the 
loss of elasticity being due to two factors, viz., 

1. Strain of the pulmonary tissue. Certain occupations, 
such as glass-blowing or performing on wind instruments, and 
certain diseases, notably asthma and chronic bronchitis, lead 
to such stretching of the lung tissue that the power of subse- 
quent contraction becomes destroyed. 

2. Weakness of the elastic framework, which is either hered- 
itary or acquired. 

Pathology, — In the hypertrophic form the alveoli become 
over-distended and this leads to atrophy of their walls, and in 
connection with the latter their blood vessels are de- 
stroyed. The lungs become so distended that when the thorax 
is opened, they fail to collapse and may even bulge forward. 

The atrophic form is in reality nothing more than a senile 
change involving the lungs among other organs. By a process 
of wasting some of the septa disappear, so that neighboring 
vesicles become fused into bullae of various sizes. On open- 
ing the chest the lungs appear small, pigmented, dry, and 
easily compressed. 

Associated Lesions. — Chronic bronchitis, hypertrophy and dila- 
tation of the right ventricle, and finally chronic venous con- 
gestion of the abdominal viscera may ensue. 

Symptoms. — 1. Dyspnea, at first slight and brought on only 
by exertion, but which finally becomes constant. 

2. Cyanosis, due to the unserated condition of the blood. 
In the earlier period of the disease the face may appear con- 
gested or slightly bluish, but later in the course cyanosis 
is marked. 

3. Cough and expectoration, due to the associated bronchitis. 
Physical Signs. — In hypertrophic cases the chest may be 

"barrel-shaped." The more important signs, however, are 
diminished fremitus, exaggerated percussion-resonance, de- 
creased vocal resonance, and a low-pitched expiratory note 
which is prolonged, even to three or four times the length 
of inspiration, and is often accompanied by rales. 



DISEASES OF THE RESPIRATORY SYSTEM. 177 

Prognosis. — The disease itself is incurable; but the dangers 
lie in its associations and complications, and much can be 
done to prevent the progress of the latter. 

Treatment.— These patients require a nourishing diet, mod- 
erate open-air exercise, and protection from cold and damp. 
Compressed air inhalations are useful, and medicinal 
measures should be adapted to the associated conditions (see 
chronic bronchitis, asthma, and gastric and cardiac diseases). 



BRONCHO-PNEUMONIA. 

(Catarrhal Pneumonia; Lobular Pneumonia.) 

Etiology. — This circumscribed inflammation of the lung tissue 
is usually a sequence of bronchitis, various septic organisms 
(staphylococci, streptococci, pneumococci, etc.) being carried 
into the air vesicles by — 

1. Extension of the catarrhal inflammation from the smaller 
tubes, by contiguity of structure, into the alveoli surrounding 
them. 

2. Sucking into the alveoli of mucus, pus, food products, 
and other irritants {.aspiration pneumonia). 

Broncho-pneumonia occurs principally in very young chil- 
dren, and occasionally in the aged, but rarely in middle life. 
It is often secondary to infectious fevers. 

Pathology. — The membrane lining the terminal bronchioles 
becomes swollen, and congested, and the tubes filled with ten- 
acious mucus {capillary bronchitis). In addition, the adjacent 
alveoli are packed with pus cells and epithelium, but 
fibrin, which is characteristic of croupous pneumonia, 
is absent. The air vesicles of portions of, or entire, lobules in 
both lungs may thus become consolidated, while other air 
vesicles, because of occlusion cf their bronchi, are collapsed 
{atelectasis) . 

On section the lung appears congested, and scattered 
through the tissue can be seen rounded areas of consolidation 
12 



178 DISEASES OF THE RESPIRATORY SYSTEM. 

about the size of peas. About these are patches of collapsed 
lung-tissue and on pressure muco-pus issues from the inflamed 
smaller bronchi. 

Symptoms. — The symptoms, which are usually added to those 
of a pre-existing disease, include : 

1. Increased frequency of respiration (50-80 per minute), 
rapid pulse (140-160), and irregular fever (101°-105°). 

2. Dyspnea and cyanosis are marked. The extraordi- 
nary muscles of respiration are brought into play, but the lips 
and face become cyanosed and the patient may sink into 
a stupor. 

3. Cough, which may have been loose and painless pre- 
viously, becomes dry, hacking, and ineffective. The expecto- 
ration is muco-purulent and scanty, or it may be entirely 
absent. 

4. Cerebral symptoms, such as delirium and convulsions, 
may by their occurrence at the outset of some cases suggest a 
meningitis, but in a few days they give place to the typical 
pulmonary symptoms. 

Physical Signs. — Scattered points of consolidation, if found, 
are distinctive ; but as a rule the solidified areas are too 
small to give rise to percussion-dulness, increased fremitus, 
etc. Auscultation may reveal patches of fine rales, not limited 
to inspiration, which are associated with the larger moist 
rales of bronchitis. 

Course. — The disease may cause death from exhaustion or 
asphyxia within a few days. If it does not, the course is 
usually protracted over two or three weeks and the disease 
finally terminates by lysis. Chronic interstitial pneumonia or 
tuberculosis may ensue. 

Diagnosis. — The diagnosis often rests upon the symptoms 
rather than the physical signs, the severity of the former in- 
dicating a process much more serious than simple bronchitis. 

Prognosis. — This is grave in all well-marked cases, the 
mortality exceeding 30 per cent. A high temperature and 
feeble pulse are ominous signs. 



DISEASES OF THE RESPIRATORY SYSTEM. 179 

Treatment. — These patients require absolute rest, highly 
nutritious liquid food, and early stimulation with some alco- 
holic. Respiratory failure should be combated by frictions 
or cold douches applied to the chest. Aconite, gelsemium, and 
ferritin plios. are valuable remedies in the earl} 7 stage, but 
increasing cyanosis requires the administration of tartar 
emetic, or apomorpliia. PhospJiorus and sulphur may be 
suggested by the presence of widespread consolidation. The 
patient should remain under treatment until it is certain that 
resolution is complete, lest tubercular infection of an un- 
resolved area occur; 



GANGRENE OF THE LUNGS. 

Etiology. — Pulmonary gangrene may be either circumscribed 
or diffuse. It is due to the organisms of putrefaction (staphy- 
lococci, leptothrix, etc.), whose activity may be secondary to: 

1. Lesions of the bronchi (putrid bronchitis), aspirated for- 
eign bodies, etc. 

2. Lesions of the lungs ; i. e., as a sequence of some pneu- 
monias and of tuberculosis. 

3. Lesions of the blood vessels (septic embolism or throm- 
bosis). 

4. Lesions of adjacent viscera (extension of a septic or gan- 
grenous process from the thoracic wall, abdomen, esophagus, 
etc.). 

5. Wounds of the thorax, extravasation of blood into the 
lung tissue being followed by gangrene. 

6. Certain general conditions, such as starvation, alcoholism, 
diabetes, nephritis, and infective fevers have been occasionally 
followed by gangrene. 

Symptoms. — Cough, dyspnea, moderate fever, and great pros- 
tration are present, and are accompanied by a profuse and 
extremely offensive expectoration. The latter settles into 
layers on standing; it may present a variety of colors, decom- 



180 DISEASES OF THE RESPIRATORY SYSTEM. 

posed blood giving it a " prune-juice" character ; and it con- 
tains pus corpuscles, elastic tissue, crystals, and micro- 
organisms. A more or less profuse hemoptysis may occur. 

Physical Signs. — These depend upon the lesions and may indi- 
cate consolidation, softening, or excavation ; they are not 
characteristic. 

Diagnosis. — By the offensive odor and other characteristics of 
the sputum. 

Prognosis. — This is generally unfavorable, death occurring 
within two weeks. Rarely the course is more prolonged, and 
occasionally the slough separates and is discharged, the result- 
ing cavity undergoes contraction, and recovery ensues. 

Treatment. — Conserve the patient's strength by administer- 
ing nourishing liquid foods and alcoholic stimulants. Use 
sprays or inhalations of creosote, carbolic acid, or terebene ; 
and internally give arsenic, lachesis, etc. 



ABSCESS OF THE LUNG. 

Etiology. — Suppuration within the lung may be due to : 

1. Pneumonia, the consolidated area undergoing softening. 

2. Tuberculosis, a caseous area becoming purulent. 

3. Bronchiectasis, ulceration involving adjoining tissue. 

4. Pyemic infarction or embolism. 

5. Suppuration of a hydatid cyst. 

6. Perforation of the lung by a malignant growth of the 
esophagus, by rupture of an empyema, or by an abscess of 
the mediastinum, of the bronchial glands, or of the abdomen. 

7. Injuries of the lung (wounds, etc.). 
The symptoms may be limited to — 
Symptoms. — 1. Fever of hectic type. 

2. Sudden expectoration of pus in large quantities. 

Physical Signs. — Examination may reveal an area of dulness, 



DISEASES OF THE RESPIRATORY SYSTEM. 181 

which may possibly simulate a pleural effusion; after expeo 
oration of the pus, the signs of a cavity appear. 

Prognosis. — Grave, but not necessarily fatal. 

Treatment. — Nourish and stimulate the patient, conserve his 
strength and use antiseptic inhalations as in cases of pulmon- 
ary tuberculosis. Consider the possibility of surgical interfer- 
ence and drainage. 



TUMORS OF THE LUNG. 

With few exceptions, a tumor of the lung, whether carci- 
noma, sarcoma, or other variety, is secondary to a similar 
growth elsewhere. As a result it usually consists of multiple 
nodules which do not attain the size and appearance of neo- 
plasms of other organs. By involving the lung tissue a tumor 
may occasion cougJi, hemoptysis, and expectoration (often 
"prune-juice"); by pressure it may cause dyspnea, perhaps 
dysphagia, and vascular obstruction ; and through invasion of 
the pleura pain may become severe. The increasing cachexia 
and the discovery of primary or secondary growths elsewhere 
may enable the physician to make a diagnosis. Treatment 
must be symptomatic and palliative. 



COLLAPSE OF THE LUNG. 

(Atelectasis.) 

Etiology. — Absence of air from a portion of the lung tissue 
may be : 

1. Congenital, respiration never having been sufficiently 
deep to innate certain portions of the lungs. 

2. Acquired, collapse having followed — 

(a) Occlusion of the upper air passages by chronic catarrh, 
enlarged tonsils, adenoids, laryngeal stenosis, etc., which 
impedes the entrance of air and so limits the expansion 
of the chest. 



182 DISEASES OF THE RESPIRATORY SYSTEM. 

(&) Occlusion of a bronchus by a foreign body, or a 
mucous plug, as in broncho-pneumonia. 

(c) Impaired chest, expansion, due to muscular paralysis 
or weakness. 

(d) Compression of the lung tissue by a pleural effusion, 
aneurism, tumor, etc. 

(<?) Pneumo-thorax. Entrance of air into the pleural 
cavity invariably causes lung collapse. 

Symptoms. — Congenital atelectasis is associated with weak- 
ness, arrested growth, and symptoms of defective oxygenation, 
such as shallow respiration, dyspnea, and tendency to cya- 
nosis. 

When lung collapse is the result of respiratory stenosis, the 
onset is apt to be sudden and marked by dyspnea, rapid 
breathing, and feeble pulse, together with inspiratory reces- 
sion of the lower intercostal spaces. Extensive collapse may 
give rise to dulness, and the breath sounds may be feeble or 
absent over the area of lung involved. 

Prognosis. — The degree of cyanosis is the best guide as to the 
gravity of the condition ; if it is increasing, the outlook is un- 
favorable. If recovery occurs, certain areas may remain un- 
expanded, and this condition favors the development of bron- 
chiectasis or tuberculosis. 

Treatment. — In a newly-born child expansion of the lungs 
may be favored by a general hot bath, by pouring cold water 
over the chest, by slapping the chest with a wet towel, or by 
bringing about artificial respiration. Rather similar methods 
are of value in the cases of pulmonary collapse attendant upon 
acute disease, notably in broncho-pneumonia. Later, attention 
must be paid to the general nutrition, and the patient should 
take respiratory exercises in the open air. 



DISEASES OF THE RESPIRATORY SYSTEM. 183 

PLEURISY. 

Etiology. — Inflammation of the pleura may be — 

1. Primary; due to bacterial infection (pneumococcus, 
streptococcus, staphylococcus, tubercle bacillus, etc.). 

2. Secondary to 

a. Local disease (extension of inflammation from the lungs 
or injury to chest wall). 

b. General diseases (nephritis, hepatic cirrhosis, cancer, 
etc.). 

Exposure to cold may induce pleurisy by lessening the re- 
sistance of the individual. 

Pathology. — 1. Dry stage. The pleural membrane becomes 
hyperemic and its surface covered with fibrinous exudate. 
{Dry> fibrinous, plastic, or adhesive pleurisy. ) 

2. Exudative stage. Should the inflammatory process con- 
tinue, a clear, straw colored serous fluid may be poured out, 
and in the latter are flakes of fibrin {sero-fibrinous or exudative 
pleurisy ; pleurisy with effusion}. 

3. Purulent stage. In time, or perhaps almost at the onset, 
pyogenic bacteria may convert the exudate into pus {purulent 
pleurisy ; empyema. ) . 

4. Chronic stage. Any pleuritic inflammation, plastic or 
exudative, which remains unresolved after several weeks, con- 
stitutes a chronic pleurisy. 

The effect of pleurisy upon the adjacent viscera depends 
upon the quantity of the effusion; if the latter is considerable, 
the adjacent pulmonary tissue becomes compressed, the heart 
is displaced toward the sound side, and if the effusion is on 
the right side the liver is displaced downward. 

Course. — 1. Resolution and absorption may occur at any 
stage, although this becomes less common with increasing 
exudation, and is rare in empyema. 

2. Dry pleurisy may occasion permanent adhesion of the 
surfaces. 



184 DISEASES OF THE RESPIRATORY SYSTEM. 

3. Unabsorbed serous effusions may remain unaltered for 
months, but they are more apt to become purulent. 

4. Small accumulations of serum or pus may be walled in 
by adhesions. 

5. Purulent effusions, if not promptly removed, may — 

a. Perforate the chest wall externally. 

b. Burrow along the muscles and point in the lumbar 
region or groin. 

c. Rupture into the esophagus or pericardium. 

d. Penetrate the diaphragm, and either enter the stomach 
or form a pus-collection between the diaphragm and 
the liver {sub-diaphragmatic abscess). 

e. Perforate the lung, the pus being discharged through 
the bronchi and air being permitted to enter the pleural 
sac (pyo-pneumothorax) . 

Symptoms. — Certain cases of pleurisy are insidious in their 
development, affording only vague chest symptoms, and incon- 
sequence they are detectable only by physical examination. 
As a rule, however, the onset of acute pleurisy is attended with: 

1. Chill or chilliness. 

2. Pain, severe and cutting, in the side; this is increased 
by any movement, even coughing or breathing, and in order 
to avoid it the patient breathes in short gasps. When the 
pleural surfaces become separated by an effusion, the pain 
lessens and disappears. 

3. Cough, dry or with scanty expectoration. 

4. Moderate fever (101°-103°) and a rapid pulse (100-120). 
Subsequently the fever declines by lysis. 

Physical Signs. — 1. Dry pleurisy is suggested by the obvi- 
ously restricted motion of the affected side, on which the 
patient usually lies in order to further restrain its movement. 
Percussion in this stage is negative; but auscultation reveals a 
grating or rubbing sound, most marked toward the close of 
inspiration and intensified by pressure of the stethoscope. 

2. Pleuritic effusion, whether serous or purulent, may 



DISEASES OF THE RESPIRATORY SYSTEM. 185 

obliterate the interspaces, restraining movement and lessening 
vocal fremitus. In addition, percussion demonstrates: 

a. Flatness over the fluid, with a sense of resistance to the 
finger during percussion. 

b. Tympanitic resonance above the level of the fluid. 

c. The upper level of the fluid is rarely horizontal ; rather 
S-shaped. 

d. The fluid may change its location slowly with a change 
in the patient's position. 

Auscultation may reveal : 

a. Feeble or absent vocal and breath sounds over the 
fluid. 

b. Egophony, at the angle of the scapula, if the amount 
of fluid is small. 

c. Bronchial or broncho-vesicular breathing over the con- 
densed lung above the fluid. 

d. Exaggerated breathing on the sound side. 

e. Displaced heart sounds. 

3. During the stage of absorption there may be : 

a. Gradual disappearance of the dulness. 

b. Gradual reappearance of the voice and breath sounds 
and of fremitus. 

c. Pleural friction may recur (redux friction). 
Diagnosis. — Pleurisy can be diagnosed with certainty only by 

recognition of its physical signs. The nature of the extrava- 
sated fluid can be determined only by exploratory puncture, 
although a marked and increasing leucocytosis suggests puru- 
lency. 

Lobar pneumonia may present dulness and bronchial breath- 
ing, but vocal fremitus and resonance are increased. Pleurisy 
is also distinguished by its upper line of dulness, the shifting 
of the latter when the patient changes his position, and the 
displacement of adjacent organs. Any doubt may be removed 
by puncturing the chest wall with a sterile needle and with- 
drawing a little fluid. 



186 DISEASES OF THE RESPIRATORY SYSTEM. 

Intercostal neuralgia and myalgia are usually distinguished 
by absence of fever as well as physical signs. The pain of the 
former is confined to one interspace, along which sensitive 
foci can be discovered. 

Prognosis. — Sudden death from thrombosis or embolism is 
possible. Excluding this contingency, the prognosis is gov- 
erned by the variety of the causative organism, the amount 
and character of the effusion, and the presence or absence of 
complications. 

1. The exciting cause. A large proportion of pleural effu- 
sions is due to the tubercle bacillus ; these cases are often 
latent and little inclined to purulency. In connection with 
every case of pleurisy it is advisable to examine the lungs, and 
especially the opposite apex, for signs of tuberculous con- 
solidation. Pneumococcic infections tend to the production 
of a mild form of empyema; and this organism is the exciting 
cause in a majority of the cases in children. Streptococcic in- 
fections, on the other hand, are severe, and the death rate is 
high (25%); these bacteria are responsible for the majority of 
the cases of empyema which occur in adults, often as a com- 
plication of other infectious diseases. It follows, therefore, 
that careful macro- and microscopic examination of the effu- 
sion, together with inoculation tests, is a great aid to definite 
prognosis. 

2. The amount and character of the effusion. Pleurisy with- 
out effusion tends to recover within a week or two. Should 
effusion occur, its tendency to become purulent varies accord- 
ing to the exciting cause, as stated. The course of empyema 
is, at best, protracted. 

3. The occurrence of complications, especially of pericarditis 
or meningitis, is of grave import. In secondary pleurisies the 
prognosis may vary according to the antecedent cause ( e. g., 
nephritis, cancer, etc.). 

Treatment. — Dry stage. Place the patient at rest. If pain is 
severe, strap the chest. Use strips of adhesive plaster three 
inches wide; apply them at the close of expiration, carrying 



DISEASES OF THE RESPIRATORY SYSTEM. 187 

each from the sound side of the vertebrae around the affected 
side to the sound side of the sternum. Begin below, and 
allow the upper to overlap the lower strips slightly. 

Administer bryonia or asclepias in uncomplicated cases. 
Associated pneumonia or phthisis may require ferritin phos., 
kali carb., phosphorus, or squills. A rheumatic cause may 
suggest the employment of colchicum or rhus ; and nephritis 
may afford indications for arsenic, cantli., or mere. corr. 

Stage of effusion. The lessening of pain as a result of 
the development of an effusion suggests a change to such 
remedies as apis, arsenic, cantharis, or sulphur. Should, 
however, the fluid fail to become absorbed after active symp- 
toms have disappeared, or should the distended pleura pro- 
duce threatening dyspnea or other symptoms, thoracentesis 
becomes imperative. Aspirate with antiseptic precautions at 
the upper border of the seventh rib in the mid-axillary line. 

Empyema. In purulent pleurisies of pneumococcal origin, 
thoracentesis may be repeated several times with a fair pros- 
pect of recovery without resort to more radical measures. 
Should the condition be of streptococcic or doubtful origin, 
however, immediate resection of a rib and drainage of the sac 
is advisable. After withdrawal of the pus, arsenic iod., chini- 
nurn ars., Jiepar, niercur., silica, and sulphur may be useful. 
Following the evacuation of the pus, healing occurs by ob- 
literation of the sac. In order to expand the collapsed lung 
tissue, vocal gymnastic exercises, such as blowing water 
from one large bottle to another, or the inhalation of com- 
pressed air, may be advised. 

PNEUMOTHORAX. 

Etiology. — Air may enter the pleural sac as the result of — 

1. Perforation of the chest zvall by wounds, by incision for 
drainage of an empyema, or by external rupture of the latter. 

2. Perforation of the pulmonic pleura by a ruptured tuber- 
cular cavity (90%), abscess, gangrene, empyema, rupture of 
the lung by violent strain, etc. 



188 DISEASES OF THE RESPIRATORY SYSTEM. 

3. Perforation of other organs which contain air, such as 
the esophagus, stomach, or colon, by an empyema. 

Pathology. — The entrance of air destroys the pleural vacuum 
and the lung shrinks by reason of its own elasticity. The 
adjacent viscera are displaced. Plural effusion soon develops, 
and according to its nature the condition becomes a hydro- 
pneumothorax or a pyo-pneumothorax. 

Symptoms. — As a rule there is a sudden onset of sharp pain 
in the chest or back, and a sensation of " something having 
given way." This is quickly followed by dyspnea and perhaps 
collapse. The very acute symptoms, if not fatal, pass off in a 
few hours. 

Physical Signs. — Inspection. The affected side is motionless, 
perhaps obviously enlarged, and the intercostal spaces are ob- 
literated and the apex beat displaced. 

Palpation. — Fremitus is absent over the affected side. 
The heart and liver are displaced. 

Percussion. — Loud tympanitic resonance is present over 
the affected side. 

Auscultation. — The respiratory and vocal sounds are inaudi- 
ble in the lower part of the chest. At the upper part of the 
chest there is faint amphoric breathing, and cough is fol- 
lowed by a ringing after-echo. If a coin placed on the back of 
the chest be struck with another coin, the examiner, listening 
in front, detects a ringing (bell) sound. The " falling drop 
sound" and "metallic tinkle" are sometimes present. 

Diagnosis. — By the physical signs. A large tubercular cavity 
usually occurs at the apex, not the base of the lung ; and in 
such a case the chest wall is sunken, not bulging, the heart is 
not displaced, and the bell sound is absent. 

Treatment. — At the outset administer stimulants if necessary; 
then strap the chest, and treat the condition simply as a 
pleurisy with effusion. 



DISEASES OF THE RESPIRATORY SYSTEM. 189 



HYDROTHORAX. 

Etiology. — A dropsical effusion into the pleural cavity is 
usually secondary to the same causes as is dropsy elsewhere, 
i. e., to heart, kidney, or blood diseases. 

Symptoms. — Dyspnea, cyanosis, and the physical signs of 
pleural effusion in both sides. 

Diagnosis. — By the history of a primary disease, the absence 
of pain or fever, the bilateral effusion, and on exploratory 
puncture the withdrawal of a thin fluid, low in specific gravity 
and poor in albumin. 

Treatment. — Treatment should be directed to the causal 
disease. If dyspnea becomes extreme, aspirate, as in cases of 
pleurisy with effusion 

HEMOTHORAX. 

Etiology. — Blood may be effused into the pleural cavity as the 
result of traumatism, aneurismal or venous rupture, and 
certain diathetic conditions, such as scurvy and purpura. 

Symptoms. — The symptoms are those of hemorrhage — 
syncope, pallor, etc. — and are severe in proportion to the 
amount of blood extravasated. Dyspnea and the physical 
signs of pleural effusion are present. 

Prognosis. — This depends upon the cause. 

Treatment. — The treatment should be symptomatic unless 
the dyspnea becomes urgent ; in that case a limited amount of 
the effusion mav be withdrawn. 



DISEASES OF THE URINARY 
SYSTEM. 



The chief symptoms of disease of the urinary organs may 
appear at first sight to have no relation to that system. In 
the investigation of these disorders it is necessary, therefore, 
that the pathological association of the various organs be kept in 
mind. The symptoms suggestive of urinary disease are of 
three classes, viz. : 

1. Symptoms, painful or otherwise, referred to the urinary 
tract (lumbar aching, pain, frequency or difficulty in mic- 
turition, etc.). 

2. Symptoms due to faulty renal elimination; i. e., uremia 
(head-ache, vertigo, vomiting or purging, convulsions, coma, 
etc.) or dropsy. 

3. Changes in the appearance of the urine (high colored, 
smoky, bloody, or very pale; scanty or profuse; containing 
various sediments, etc.). 

In a certain proportion of cases the patient is induced by 
these symptoms to seek a physician; but more often the indi- 
cations of a renal disorder remain vague and unnoticed. The 
effects of chronic nephritis in particular are so far reaching, pro- 
ducing disturbances of the circulatory, respiratory, digestive 
or nervous systems, that it is the rule to investigate the urine 
repeatedly in every case of persistent ill health. 

Interrogation of the Patient. — Should suspicion be directed to 
the urinary system, the patient should be questioned as to : 

1. A family history of gout, paralysis, heart, or kidney 
disease. 



192 DISEASES OF THE URINARY SYSTEM. 

2. A personal history of acute infections, syphilis, lead 
poisoning, gout, prolonged suppuration, or previous renal 
disease. 

3. Has he any pain in the lumbar region ? Any pain in 
micturition? If so, is it before, during, or after urination? 
What is its character and where is it felt ? Is it aggravated 
by movement? Was there ever a sudden attack of pain 
shooting down into the groin? 

Does he have to arise at night to micturate ? Is there 
increased frequency of micturition ? 

Is the face ever puffy in the morning, particularly beneath 
the eyes ? Do the ankles swell ? 

4. Does he complain of drowsiness, headache, vomiting, 
diarrhea, dyspnea, dimness of vision, convulsions, or paralysis ? 
Inquire also as to the condition of the digestive system. 

5. The urine: is it altered in quantity? In color? Is it 
clear or cloudy when passed? Is there ever any blood in it, 
and if so, when? 

Physical Examination of the Kidney. — In order to palpate the 
kidney, sit by the patient on the side to be examined, and 
place one hand below the last rib behind and the other over 
the lower part Of the hypochondriac region in front. Let the 
patient's knees be drawn up and his shoulders raised. Then 
ask him to draw a long breath, and during inspiration follow 
down the receding abdominal wall with the hand in front. If 
the patient is not too fat, the lower part of the kidney can 
thus be felt even in health. 

The kidney moves very slightly with respiration. Should it 
be freely movable in almost any direction, it constitutes a 
" floating kidney." A distended gall-bladder may be mistaken 
for the kidney, but the former when pushed back from the 
abdominal wall springs forward again, while the kidney often 
disappears for a time, and is seized with difficulty. Moreover, 
the kidney can be pushed down towards the pelvis and held 
there, but the gall-bladder moves up again during expiration. 

An enlarged left kidney might be mistaken for the spleen, 



DISEASES OF THE URINARY SYSTEM. 193 

but the edge of the latter is sharp while the kidney is always 
rounded. Often the colon is felt as a soft yielding structure 
in front of the kidney, never in front of the spleen. 

Enlargement of the kidney, due to pyelitis, hydronephrosis, 
tuberculosis, a malignant neoplasm, a cyst, or an abscess, may 
be palpable. Fluctuation in the mass suggests hydronephro- 
sis or a cyst, while hardness and nodulation signify malignant 
disease. 

Only extreme enlargement of the kidney can produce bulg- 
ing of the abdominal wall sufficient to catch the eye on inspec- 
tion. Percussion is much less valuable than palpation. 

EXAMINATION OF THE URINE. 

By examination of the urine we obtain evidence as to: 

1. The progress of metabolism. For example, urea, the 
result of albuminoid disintegration, is excreted in the urine, 
and by determining its amount we can estimate the relation 
of nitrogenous expenditure to income. Sugar, appearing in 
the urine as a result of abnormal metabolism, affords positive 
•evidence of certain grave pathological conditions. 

2. The condition of the kidneys and bladder. Albumin and 
certain histologic elements, absent in normal urine, appear in 
cases of kidney disease. Disease of the bladder may occasion 
urinary decomposition. 

3. The condition of other organs. Diseases of the liver may 
occasion the escape into the blood and thence into the urine 
of biliary coloring matter. Diseases of the small intestine 
are frequently accompanied by indicanuria. 

The method of collecting the urine for examination is im- 
portant. If possible, the patient should preserve the entire 
quantity passed during a period of twenty-four hours in a 
clean, closed vessel (preferably a large, well-corked bottle), 
and keep it in a cool place to prevent decomposition. At the 
•end of the period the quantity should be accurately measured 
in ounces or cubic centimetres, and about four ounces should 
13 



.1.94 DISEASES OF THE URINARY SYSTEM. 

be brought to the physician for examination. If the micro- 
scopical examination cannot be made at once, a few drops 
of formalin or a few grains of salicylic acid may be added as 
a preservative; but this may invalidate chemical tests. 



PHYSICAL EXAMINATION OF THE URINE. 

1. Quantity. — This may be modified by the sex or bulk of the 
patient, the quantity of food and drink, and the amount of 
excretion by the skin, bowels, etc. The average quantity is 
about three pints in twenty-four hours ; less than one or more 
than five pints usually indicates disease. The quantity is de- 
creased as a result of free sweating, diarrhea, the gouty dia- 
thesis, and acute fevers, and in acute and some forms of 
chronic nephritis. It is increased in diabetes, chronic inter- 
stitial nephritis, and hysteria. 

2. Color. — The normal color is yellow. The smaller the 
quantity the greater the concentration, and therefore the 
deeper the color. It is brown, with yellow foam, when it con- 
tains biliary coloring matter ; when it contains blood it may be 
red, or intimate admixture of the latter may render it smoky ; 
and poisoning with carbolic acid or creosote may render it 
black. Very pale urine is found when the quantity is excess- 
ive, as in diabetes or chronic interstitial nephritis ; and it may 
also occur in hysteria or as a result of excessive drinking. 

3. Reaction. — The chemical reaction is ascertained by means 
of litmus paper. Normally it is acid. If it is sharply so, 
intensely reddening the blue litmus, the possibility of sugar is 
suggested. Should it be alkaline, the red litmus becoming 
blue, notice whether the red color returns on drying the paper ; 
this indicates a volatile alkali, and if the urine be freshly voided 
suggests a chronic inflammatory condition of the lower urinary 
tract. If, however, the blue color persists on drying, the 
alkali is fixed and indicates unusual alkalinity of the blood, 
which may possibly be due to fasting, dyspepsia, a vegetable 
diet, or to alkaline waters or medicines. 



DISEASES OF THE URINARY SYSTEM. 195 

4. Specific Gravity. — This is taken by means of a urinometer. 
Normally it is between 1015 and 1025. A very loiv specific 
gravity is found in all cases where the quantity of urine is 
large, and in diabetes insipidus, amyloid kidney, and chronic 
interstitial nephritis. It is high in the concentrated urine of 
fever, the scanty urine of renal or cardiac dropsy, or as a re- 
sult of a limited consumption of fluids ; and it is especially 
high, and at the same time Increased in quantity, in cases of 
diabetes mellitus. 

The proportion of solids in any given specimen of urine may 
be calculated by multiplying the last two figures of the specific 
gravity by 2.2 (Loebish's coefficient). The result indicates 
the amount of solids in every 1000 parts. 

5. Cloudiness. — Normal urine is quite clear. Turbidity in any 
degree is abnormal, its significance being judged according to 
the chemical reaction present. Cloudiness in acid urine may 
be due to urates, which will be dissipated on heating in a test- 
tube, or to histological elements, which must be detected 
microscopically. Cloudiness in alkaline urine may be due to 
the presence of phosphates, rarely calcium oxalate, and will 
then disappear on the addition of a few drops of acid. Should 
it persist, it is due to organic matters requiring microscopical 
examination for their detection. 

A milky turbidity of the urine may be due to the presence of 
chyle {cJiyluria), and in that case after the urine has been 
allowed to stand for a time a light coagulum settles to the 
bottom and a creamy pellicle of fat rises to the surface. This 
condition is the result of some communication between the 
lymphatic system and the urinary tract. While rare in this 
climate, chyluria is not uncommon in the tropics, and is there 
associated with the presence of the filaria sanguinis hominis. 



196 DISEASES OF THE URINARY SYSTEM. 

CHEMICAL EXAMINATION OF THE URINE. 

The routine chemical examination of urine implies estima- 
tion of the amount of urea in the twenty-four hours's urine, 
and qualitative tests for albumin and sugar. Examination for 
other substances is reserved for special contingencies. 

NORMAL CONSTITUENTS. 

1. Urea, the chief end-product of albuminoid disintegration, 
is by far the most important organic element dissolved in the 
urine. Only by the amount of urea excreted in each period 
of twenty-four hours can the physician judge as to the extent 
to which the kidneys are performing their function. Normally 
the amount ranges from 300 to 600 grains (20 to 40 grammes) 
daily in a man of average weight (150 pounds). Its persistent 
diminution below 250 grains strongly suggests kidney disease, 
and if it falls below 175 grains daily, uremia is to be appre- 
hended. It is decreased also in acute yellow atrophy of the 
liver. It is increased in fever, anemia, and poisoning by arse- 
nic and other drugs. 

For clinical purposes the best test is that with a sodium 
hypobromite solution, using Doremus' ureometer. To ten c.c. 
of a caustic soda solution (3 ounces of caustic soda in 8 ounces 
of distilled water) add 1 c.c. of bromine, and mix thoroughly; 
then add an equal quantity of water, and fill the bulb of the 
instrument with the mixture, inclining it until the solution fills 
the long arm. Into the latter slowly discharge 1 c.c. of the 
urine. Immediately nitrogen gas is evolved as the result of 
decomposition of the urea and collects at the top of the tube. 
When no further evolution of gas occurs, read off the quantity 
as marked by the numbers on the tube, each of which repre- 
ents the fractions of a gramme of urea per c.c. of urine, of 
which 0.02 is about normal; multiplying the figure by 100 
gives the percentage of urea. From this the total daily ex- 
cretion can easily be reckoned. 



DISEASES OF THE URINARY SYSTEM. 197 

A mixture of 25 c.c. of Labarraque's solution with 5 c.c. of 
a 20 per cent, potassium bromide solution may be substituted 
for the usual hypobromite solution, but the reaction, while 
accurate, is much slower. 

2. Uric acid, like urea, is a product of nitrogenous meta- 
bolism, and is normally excreted in the urine in small amounts 
(0.4 to 1.4 gramme daily). Frequently it is precipitated in 
the form of characteristic crystals as the result of high acidity 
of the urine, its poverty in mineral salts, its long standing, 
or because of the excessive amount of the uric acid present. 
The mere occurrence of such deposit does not necessarily indi- 
cate that an excess of the acid is present. Being a normal 
constituent of urine, chemical demonstration of its presence is 
of no clinical significance, and its quantitative determination 
is rarely demanded. Its important relation to the gouty dia- 
thesis may, however, render such an analysis desirable ; the 
process, which is somewhat intricate, is detailed in the special 
works on urinalysis. 

3. Indican, normally present in the urine is small quanti- 
ties, becomes greatly increased as the result of the extensive 
decomposition of albuminous substances in the small intestine, 
e. g., in cases of peritonitis or intestinal obstruction. It is 
increased, but in lesser degree, in connection with suppurative 
processes and nervous diseases. For its detection, pour 4 c.c. 
of hydrochloric acid into a small flask and while stirring add 
from 10 to 20 drops of urine. If the proportion of indican 
present is about normal, the resulting color will be yellow; if 
excessive, the acid will turn violet or blue. If no coloration 
appears in a minute or two, there is certainly no excess 
present. 

4. Xanthin, creatinin, hippuric acid, various pigments, etc., 
while present in normal urine, are rarely of sufficient import- 
ance to demand chemical identification. The quantitative 
determination of the ethereal sulphates in their relation to the 
total sulphates has been recommended as a reliable index to 
the intensity of putrefactive changes within the intestine. 



198 DISEASES OF THE URINARY SYSTEM. 

The technique of these tests will be found in works devoted 
to urinary analysis. 

5. Inorganic constituents of the urine, chiefly chlorides, carbon- 
ates, sulphates, and phosphates in combination with ammo- 
nium, potassium, calcium, and magnesium, are not, as a rule, of 
clinical importance. The chlorides are diminished in all acute 
febrile diseases, gradually increasing after the crisis ; the latter 
may, therefore, constitute a favorable prognostic sign. In 
pneumonia the chlorides may totally disappear from the urine, 
and this is often an ominous sign. Their presence and per- 
centage is best determined by the centrifugal method. Fill 
the percentage tube which accompanies the centrifuge with 
urine to the 10 c.c. mark, add 15 drops of nitric acid, and 
fill to the 15 c.c. mark with silver nitrate solution (3j to 3j). 
Mix the contents by inverting the tube, revolve it at moderate 
speed for three minutes, and the bulk percentage of the preci- 
pitated chlorides can be read from the scale on the side of the 
tube. Normally it is from 10 to 12 per cent. 



PATHOLOGICAL CONSTITUENTS. 

Albumin may be present in the urine as a result of lesions of 
the renal epithelium, blood changes, and alterations in blood 
pressure ; one or all of these conditions may be present in a 
single case. Nominal traces of albumin may be found in any 
urine by delicate testing, and a physiological albuminuria may 
follow richly albuminoid meals, intense physical strain, or a 
hot bath. If the urine contains blood or pus, the albumin of 
the plasma is dissolved out and filtration will not remove it; 
this constitutes a spurious albuminuria. 

Pronounced and persistent albuminuria is, however, indicative 
of a renal lesion, and its discovery should be followed by system- 
atic search for confirmatory evidence in the form of casts. The 
specimen of urine selected for this test should be freshly 
voided, preferably not that passed on awakening in the morn- 
ing, and it must be carefully filtered. 



DISEASES OF THE URINARY SYSTEM. 199 

1. Heat Test. — Boil the urine in a test-tube. Should cloudi- 
ness appear, which is not removed by the addition of a drop 
or two of acetic or nitric acid, albumin is present. 

Or, add two drops of acetic acid to a test-tube full of urine 
and boil the upper portion. Cloudiness of the boiled portion 
indicates albumin. 

2. Nitric Acid Test (Heller's,). — Hold a test-tube contain- 
ing a small quantity of pure nitric acid in an almost horizontal 
position, and allow a similar quantity of urine to trickle gently 
down the side of the tube and float upon the surface of the 
acid. An opalescent zone at the point of contact indicates 
albumin; if it is not at once perceptible, set the tube aside and 
examine it again in half an hour. 

3. Fej'rocyauic Test. — Into a test-tube pour from 15 to 30 
drops of acetic acid, and add twice that quantity of potassium 
ferrocyanide solution (5%). Add sufficient urine to half fill 
the tube, close the end of the latter with the thumb and invert 
it three or four times in order to mix the reagents, and then 
stand it in a good light. If even a trace of albumin is present, 
a milk-like turbidity will appear within two minutes. 

4. Picric Acid Test. — Upon the surface of some urine in a 
test-tube float a small quantity of a saturated watery solu- 
tion of picric acid ; if there is no opacity at the level of con- 
tact, albumen is certainly absent. 

5. Quantitative estimation of albumen is best accomplished 
with the centrifuge. Fill the graduated tube with urine to 
the 10 c.c. mark, add 3 c.c. of potassium ferrocyanide solution 
(10%), and 2 c.c. of acetic acid, and mix them by inverting the 
tube several times. Revolve until all the albumin has settled; 
each yV c.c. represents 1% of albumin. 

Sugar may appear in the urine as the result of cerebral or 
bulbar disease, etc., but its persistence in detectible quantity 
is the principal and sometimes the only symptom of diabetes 
mellitus. 

1. Reduction Tests. — Grape sugar has the property of reduc- 
ing certain substances (e. g., copper oxide) to a lower state of 



200 DISEASES OF THE URINARY SYSTEM. 

oxidation. Of several tests based upon this fact (Trommer's, 
Moore's, Fehling's) the best is : 

Haines' 7>.?/.— Take pure copper sulphate, 30 grains; dis- 
tilled water, T /z ounce ; make a perfect solution and add pure 
glycerine, Y* ounce ; mix thoroughly, and add 5 ounces of 
liquor potassse. 

Gently boil about one drachm of this solution in a test-tube, 
add from 6 to 8 drops of the urine, and again boil. If sugar is 
present, a dense yellowish precipitate appears. 

2. Fermentation Test. — As a result of the fermentation set 
up by yeast, grape sugar is broken up into alcohol and carbon 
dioxide. This method is most reliable and should be used in 
all doubtful cases. By using the saccharimeter of Einhorn 
the test is made quantitative. Mix 10 c.c. of the urine in a 
test-tube with a bit of compressed yeast the size of a bean, 
shake well and pour the mixture into the fermentation tube. 
Incline the instrument until the fluid completely fills the gradu- 
ated tube, and stand it in a warm room for twenty-four hours. 
If sugar has been present, carbonic acid will then have col- 
lected in the tube, the graduations indicating the percentage 
of the sugar. 

This test is not reliable when more than 1 per cent, 
of sugar is present. On this account it is well to previously 
dilute the urine ; a specific gravity of 1018 to 1022 necessitates 
double dilution, 1022 to 1028 a fivefold dilution, and 1028 to 
1038 a tenfold dilution. Tip's requires, of course, a corre- 
sponding multiplication of the result obtained by the test. 

Accurate quantitative results may be obtained by titration 
with Fehling's or Purdy's solution, or by the use of the polari- 
scope. 

Blood may color the urine either by the admixture of its cor- 
puscles (hematuria) or by the presence of its free coloring 
matter in solution (hemoglobinuria). The distinction is best 
made by microscopic examination. 

Bile in the urine has the same significance as jaundice else- 
where. Icteric urine is dark brown in color with yellow 



DISEASES OF THE URINARY SYSTEM. 201 

foam. If a few drops of such a urine and a few drops of fum- 
ing nitric acid be permitted to flow together on a white plate, 
at the point of contact a play of color— green, blue, violet, 
red, and yellow — may be observed (Gmellins testK 

Acetone appears in the urine abundantly after extensive albu- 
minoid disintegration, such as occurs in high fever, severe 
anemia, and some cases of cancer. In severe and advanced 
cases its occurrence may immediately precede the more dan- 
gerous diaceturia. 

Test. — Dissolve 20 grains of potassium iodide in a drachm 
of liquor potassse and boil; then place the solution in a test 
tube and upon its surface float the suspected urine. At the 
point of contact phosphates are precipitated and if acetone is 
present yellow points of iodoform appear. 

Diacetic acid is always of serious significance, and its appear- 
ance in the urine of diabetics is usually a prelude to coma and 
death. It may occur also at the height of acute fevers or as 
the sole evidence of an auto-intoxication. In either case it 
is of grave significance. 

Test. — To some freshly-voided urine add a few drops of a 
ferric chloride solution. If phosphates are precipitated, filter 
them off, and to the filtrate add a few drops more of the ferric 
chloride solution. A dark red color, which disappears on 
boiling, indicates the presence of diacetic acid. 



MICROSCOPICAL EXAMINATION OF THE URINE. 

Sedimentation of the urine was accomplished formerly by 
setting aside the specimen in a carefully-covered conical glass 
for twenty-four hours. This method may still be pursued, but 
in general it has been abandoned for the centrifuge, by the 
use of which a profuse sediment can be obtained in a few 
minutes, and if necessary the examination can be completed 
before the patient leaves the consulting room. 

Before sedimentating the urine ascertain its reaction, and if 
it is cloudy discover whether the turbidity is due to phos- 



202 DISEASES OF THE URINARY SYSTEM. 

phates or urates. If the latter are present in an amount suffi- 
cient to obscure the other sediments it may be well to heat the 
urine moderately in a test tube, then sedimentate it rapidly, 
and examine the specimen on a warmed slide before cooling 
permits the reappearance of the urates. 

In using the centrifuge fill the tube with urine to within half 
an inch of the top, and see that the other tube is filled to a 
corresponding point. Then revolve the tubes at moderate 
speed for two or three minutes. As a rule, this affords suffi- 
cient sediment, but if on inspection the amount of the lat- 
ter appears insufficient, withdraw the upper portion of the 
urine without disturbing the sediment, fill the tube again with 
fresh urine, and rotate as before. If necessary this procedure 
can be repeated several times, or until enough sediment has 
been secured. Then carry the point of a pipette to the bot- 
tom of the tube and draw up about 5 drops of the sediment, 
and place it upon a clean slide. A cover-glass is unnecessary. 
Examine first with a low power, J or f objective, reserving the 
higher power for a more detailed inspection of the objects 
discovered. 



CHEMICAL SEDIMENTS. 

In acid urine the following sediments occur: 

Amorphous urates (quadriurates of sodium, potassium and 
ammonium) appear as a reddish, granular looking sediment, 
the so-called "brick dust deposit." It is readily dissolved by 
heat, while the addition of a little hydrochloric acid will cause 
uric acid to crystallize out. The presence of amorphous 
urates indicates only acidity and concentration of the urine. 

Uric acid appears as crystals yellow or brown in color, in 
consequence of the urinary pigment absorbed by them, and 
varying in shape from rhombic prisms to cylinders, rosettes, 
etc. It becomes re-dissolved on the addition of potassium 
hydrate, but not on heating, and re-crystallizes out on the 
addition of hydrochloric acid. 



DISEASES OF THE URINARY SYSTEM. 203 

Uric acid sediments are often the result of febrile states 
accompanied by concentrated and therefore more acid urine. 
Their persistence, however, suggests an actual excess of uric 
acid; and on account of the importance of the latter in its re- 




FiG. 16 — Uric Acid Crystals. (Salinger-Kalteyer.) 

lation to the uric acid diathesis, repeated quantitative analyses 
may be desirable. 

Calcium oxalate appears in the urine as colorless octahedral 
crystals or minute dumb-bells. A small number of these may 




FiG. 17 — Various Forms of Calcium Oxalate Crystals. (Salinger-Kalteyer.) 

be normal ; an excessive quantity possesses a significance allied 
to that of uric acid (oxalic acid diathesis). 

Cystin rarely appears in the urine. When present, it as- 



204 



DISEASES OF THE URINARY SYSTEM. 



sumes the form of hexagonal crystals which are readily soluble 
in ammonia. 

Leucin is sometimes seen in the form of yellowish refractive 
spheres which resemble oil globules, but unlike the latter are 
insoluble in ether. Tyrosin crystallizes in colorless sheaves of 
fine needles. These two sediments appear in the urine, usually 
together, as a result of phosphorus poisoning or acute yellow 
atrophy of the liver. 

In alkaline urine the following sediments occur : 




Fig. 18 — Crystals of Triple Phosphate. ( Salinger -Kalteyer.) 

Ammonio-magnesium (-• ^triple") phosphate, colorless coffin- 
shaped crystals readily soluble in acetic acid. 

Calcium phosphate, either " amorphous," i. e., small colorless 
granules deposited as a white sediment in alkaline urine, or 
rarely "stellar phosphate," crystalline rods arranged in stellar 
or rosette form. 

Ammonium urate, dark-brown spherical masses studded with 
fine spicula — "thorn-apple crystals." 

These alkaline deposits indicate nothing but the decomposed 
state of the specimen of urine. 



DISEASES OF THE URINARY SYSTEM. 205 



ANATOMICAL SEDIMENTS. 

Blood corpuscles may appear in the urine ; they may exhibit 
the characteristic reversal of light and shade at their margins 
while the lens is being focussed up and down, but the)' are 
pale and do not form rouleaux. Hematuria is always patholo- 
gical, indicating hemorrhage from the kidney, ureter, bladder, 
or urethra ; and among the possible causes of the latter may 
be included congestion, inflammation, cancer, tubercle, syphilis, 
stone, and traumatism. As a rule, the brighter the color of 
the blood, the nearer its source to the meatus ; and the more 
intimate its admixture with the urine and the darker its color, 
the higher in the urinary tract is its source. Associated symp- 
toms and physical signs will aid in localizing the lesion. Blood 
pigment may also appear in the urine {hemoglobinuria) turn- 
ing it dark or smoky in color. It is the result of corpuscular 
destruction within the blood vessels, the pigment being set 
free and eliminated by the kidneys ; the causes are usually 
toxic (poisoning by carbolic acid, potassium chlorate, etc., or 
infectious fevers, such as malaria, 3-ellow fever, etc.), but it 
may occur as a specific disease (paroxysmal hemoglobinuria). 
It is distinguished from hematuria by the failure to discover any 
corpuscles on microscopical examination, while the guaiac 
test, which consists in overlaying the urine with equal parts of 
tincture of guaiac and hydrogen dioxide, shows hx an indigo- 
blue ring above the white deposit that blood-pigment is 
present. 

Pus corpuscles (leucocytes) may appear sparsely in normal 
urine, but if abundant (pyuria) they indicate suppuration in, 
or rupture of an abscess into, some point in the urinary tract. 
In women, however, the pus may be due to leucorrhea, in 
which case it is associated with flat epithelial cells from the 
vagina. Otherwise, purulent urine, if acid, generally comes 
from the kidne) r s; if alkaline, from the bladder. The pus cor- 
puscles appear as circular, granular discs, with one or more 
nuclei. In the fresh state they exhibit ameboid movement, 
but in the urinary sediment they are usually dead. 



206 DISEASES OF THE URINARY SYSTEM. 

Epithelium is found in small amount in every specimen of 
healthy urine, but as a result of diseased states it may be 
thrown off in much larger quantity. Formerly it was believed 
that the special form of epithelial cell found in the urine was a 
valuable aid in locating the lesion, but this is only partly true. 
Three varieties of cells may be recognized, viz. : 

Round cells, derived from the uriniferous tubules and the 
deep layers of mucous membrane in the renal pelvis, bladder 
and male urethra. 

Columnar cells, irregular and elongated, mostly derived 
from the superficial layer of mucous membrane in the renal 
pelvis. 




Fig. 19 — Squamous Epithelium, as it Appears in the Urine. (Upper Half.) 
Epithelial Casts. (Eower Half. ) (Salinger-Kalteyer. ) 

Flat cells, large and somewhat rounded, derived chiefly 
from the bladder and vagina. 

Casts are probably due to the exudation into the renal 
tubules of the coagulable portion of the blood in which de- 
tached and altered anatomical elements become entangled. 
They are washed from their tubular mold by the urine, in 
which they appear as : 

Hyaline casts, homogeneous, transparent structures, often 
with ill-defined contours. Their presence is not positive proof 
of nephritis; they are present in association with other casts in 
all forms of renal inflammation, and occur alone in cases of 



DISEASES OF THE URINARY SYSTEM. 207 

contracted kidney, passive hyperemia of the kidney, and 
fevers. A larger form, yellowish in appearance and stained 
brown by the addition of iodine, is the so-called "waxy cast" 
which was formerly supposed to indicate amyloid degeneration 




Fig. 20 — Hyaline Casts. (Salinger-Kalteyer.) 

of the kidney, but is now known to occur in all forms of 
chronic nephritis. 

Epithelial casts, consisting of epithelial cells agglutinated 
into a cylinder, are the result of nephritis involving the tubules. 




Fig. 21 — Coarse and Fine Granular Casts. (Salinger-Kalteyer.) 

Granular casts result from the metamorphosis of epithelium 
or blood cells; they may be light or dark and coarsely or 
finely granular. Their presence indicates a chronic degenera- 
tive lesion of the kidney. 



208 DISEASES OF THE URINARY SYSTEM. 

Blood casts, composed of agglutinated corpuscles, indicate 
hemorrhage into the tubules. 

Pus casts occur rarely in connection with suppurative renal 
disease. 

Many casts are of a composite type, granular matter, epi- 
thelial cells or blood being embedded in a hyaline matrix. 
Cylindroids, long, ribbon-like mucous threads of uncertain sig- 
nificance, must not be mistaken for casts; and epithelial cells, 
corpuscles, urates, etc., may be grouped into false casts which 
can be distinguished only by experience. 




Fig. 22 — Cylindroids. (Salinger-Kalteyer.) 

UREMIA. 

Etiology. — The condition is one of toxemia due to the reten- 
tion of certain waste matters normally excreted by the kid- 
neys. 

Symptoms may appear abruptly {acute uremia) or develop 
gradually {chronic uremia). They may be limited to one or 
two phenomena, such as headache and dyspepsia, or may in- 
clude the more pronounced forms. 

Cerebral Symptoms. — Headache, persistent drowsiness, 
vertigo, delirium, coma, convulsions, sudden blindness (often 
without retinal change), and transient paralyses. 

Respiratory Symptoms. — Dyspnea ("uremic asthma"), 
Cheyne-Stokes respiration. 



DISEASES OF THE URINARY SYSTEM. 209 

Abdominal Symptoms. — Dyspepsia, pain, nausea, vomiting 
hiccough, diarrhea, or constipation. 

General Symptoms. — Cramps, particularly in the calf-muscles 
at night ; itching of the skin. 

Diagnosis. — A knowledge of the renal condition will lead to 
instant recognition of the cause of these symptoms. In 
doubtful cases, the patient being comatose or in convulsions, 
it may be noted that the breath has the odor of urine, the 
arterial tension is high, the urine is suppressed, and the small 
amount obtainable from the bladder by catheterization con- 
tains albumin and casts. *- 

Prognosis. — Grave. From the uremia of acute nephritis per- 
manent recovery may occur ; in cases of chronic nephritis re- 
cover} 1 , while possible, can be but temporary. 

Treatment. — Stimulate the organs of elimination ; the skin, 
by the use of warm baths or heat (hot air, hot bottles) ; the 
bowels, by cathartics (croton oil, two drops in a drachm of 
olive oil or glycerine ; elaterium, gr. % in solution); and the 
kidneys themselves, by the administration of cuprum ars., five 
grains of the second decimal trituration, repeated in one hour 
if necessary, or continued in grain doses every two hours if the 
symptoms are not acute. Mercurius corrosivus may be simi- 
larly useful at times. 



ACUTE HYPEREMIA OF THE KIDNEY. 

Etiology. — Renal congestion ma} 7 be due to : 

1. Poisons (cantharides, turpentine, arsenic, etc.). 

2. Infections (common to most fevers). 

3. Compensation (after removal of one kidney). 

4. The first stage of nephritis. 

Symptoms. — Scanty urine of high specific gravity and dark- 
ened color generally constitutes the only evidence of renal 
congestion. Unless inflammatory changes (acute nephritis) 
supervene, no direct treatment is necessary. 
14 



210 



DISEASES OF THE URINARY SYSTEM. 



CHRONIC HYPEREMIA OF THE KIDNEY. 

Etiology. — Passive congestion results from venous obstruc- 
tion, which may be : 

1. Systemic (chronic disease of heart, lungs, or liver). 

2. Local (obstruction to renal veins by thrombus or pressure 
of tumor). 

Pathology. — The kidney becomes enlarged, firm, smooth, and 
bluish-red (cyanotic induration), the veins are engorged with 
blood, and nephritis may result finally. 

Symptoms. — The urine is scanty, of high specific gravity, and 
contains some albumin and a few narrow hyaline casts. The 
general symptoms are those of the primary disease. 

Diagnosis. — Passive congestion of the kidney accompanies all 
uncompensated valvular heart lesions. It must be distin- 
guished from chronic interstitial nephritis, q. v. 

Treatment must be directed to the primary lesion. 



THE CLASSIFICATION OF BRIGHT'S DISEASE. 



Nephritis, -j 



Chronic. 



Acute. \ 



Parenchymatous. 



Interstitial suppura- 
tive or pyelo-ne- 
phritis. 



C Recovery usual; 
death not infre- 
quent; may termi- 
nate in chronic 
parenchymatous 
form. 

Acute surgical kid- 
ney; rare; due to 
ascending i n f e c- 
tion. 

i. " Large white 
kidney," which 
may become 
2. " Small white kid- 
ney " or may be 
associated with the 
[ 3. Amyloid kidney. 

Interstitial suppurative or pyelo-nephritis 
(chronic surgical kidney.) 

f 1. Primary. 
2. In association with 
general arterio- 
sclerosis. 



Parenchymatous. 



Imterstitial (n o n 
suppurative.) 



DISEASES OF THE URINARY SYSTEM. 211 

ACUTE PARENCHYMATOUS NEPHRITIS. 

(Acute Diffuse, Desquamative, Tubal or Catarrhal Nephritis.) 

Etiology. — Acute inflammation of the renal Parenchyma re- 
sults from the passage through the kidney of irritants, in- 
cluding — 

1. Bacterial toxins, in connection with an acute infectious 
disease (scarlatina, etc.). 

2. Bacteria. 

3. Chemical poisons (cantharides, turpentine, and other 
substances eliminated by the kidneys). 

4. Exposure to cold and damp, probably through its effect 
on metabolism, may indirectly induce nephritis. 

Pathology. — The kidney becomes swollen and bright red in 
color at first; later it is paler and and mottled. The capsule is 
non-adherent. The inflammatory process consists of — 

1. Hyperemia, intense in character, which causes enlarge- 
ment of the kidney even to the point of rupturing its capsule; 
and by pressure occludes the tubules, prevents excretion, and 
may rupture the blood vessels, with resulting hematuria. 

2. Exudation into the tubules, occluding their lumen. The 
desquamated epithelium together with blood corpuscles be- 
comes enmeshed in this exudate and the whole appears in 
the urine as a cast. 

3. Hyperplasia of the connective tissue begins at the end of 
30-40 days. 

Symptoms. — 1. Urinary changes. 

a. Reduction in the quantity, even suppression. 

b. Presence of albumin in large quantities. 

c. Presence of blood. A large quantity causes a dark, 
smoky appearance of the urine; but a small amount 
requires the microscope for its detection. 

d. Presence of casts (epithial, granular, blood, and 
hyaline). 



212 DISEASES OF THE URINARY SYSTEM. 

e. Reduced solids. The decrease in the quantity of urine 
renders it concentrated and of high specific gravity 
(1020-1040), but the total daily elimination of solids is 
much lessened. 

2. Rapid and progressive anemia. 

3. Dropsy. This usually begins about the face, but general 
anasarca may ensue. 

4. G astro-intestinal disturbances. Nausea and vomiting are 

quite common. 

5. Uremia may develop at any time. 

Duration. — Acute nephritis tends to recover in from one to 
six weeks; but it may merge into a sub-acute or chronic 
form. 

Diagnosis. — The urinary examination is conclusive. Acute 
nephritis may occur in the course of chronic nephritis, but the 
cardio-vascular changes will indicate the pre-existence of the 
latter. The simple albuminuria of fever shows neither blood 
nor epithelial casts in the urine. 

Prognosis. — Guardedly favorable. Uremic symptoms and 
suppression of urine are unfavorable signs. 

Treatment. — 1. Absolute rest in bed, with liquid diet. 

2. Reduction of the renal congestion may be favored by 
stimulating the skin (hot baths, 105°-120°, for ten or twenty 
minutes once or twice daily; or dry cups may be applied to 
the back); and by relaxing the bowels (Hunyadi water). 
Pure water in large quantities should be taken by the patient. 

3. Medicines. Aconite is generally indicated in the early 
stages, while renal congestion is intense; occasionally veratrum 
viride may be preferable. In children symptoms of cerebral 
irritation, such as convulsions, with dry skin, etc., may indi- 
cate belladonna. 

Later, in the exudative stage, rhus toxicodendron is often 
clearly indicated and may be the only remedy required. 
Should the degree of dropsy be considerable, however, 
preference should be given to cantharis ; while cases with 



DISEASES OF THE URINARY SYSTEM. 213 

little dropsy but much blood in the urine are benefited by 
turpentine. 

In more advanced cases, general anasarca requires the ad- 
ministration of mercurius corros., apis, or arsenic. It may be 
necessary to remove the dropsical accumulation by mechanical 
means (capillary drainage) or by the administration of 
diuretics (infusion of digitalis or of apocynum, 20-30 minims 
every three hours). Anemia may justify the use of iron prep- 
arations. 

CHRONIC PARENCHYMATOUS NEPHRITIS. 

( Chronic Diffuse, Tubal, or Catarrhal Nephritis. ) 

Etiology. — A chronic inflammatory process particulary affect- 
ing the renal parenchyma may be : 

1. A sequel of acute nephritis. 

2. A result of the same cause long continued, i. e. y passage 
of some irritant (bacterial, toxins, alcohol, uric acid, etc.). 

3. A complication of pregnancy. 

Pathology.— The disease is primarily an inflammation of the 
tubular epithelium, with a secondary interstitial fibrosis. Two 
stages are distinguishable, viz., 

1. The large white kidney. The tubular epithelium is 
swollen and degenerated, the lumen of the tubules is more or 
less occluded with debris, and bands of interlobular connective 
tissue form; as a result the arteries are compressed and the 
cortex is thickened and anemic, while the pyramids are dark 
in color. 

2. The small white kidney. Later, contraction of the con- 
nective tissue renders the organ smaller and lobulated. The 
tubes are choked as before, and their constriction occasions 
minute retention-cysts. 

In the first stage the capsule strips off easily, though some- 
times it drags a little of the parenchyma with it; in the second 
stage it is largely adherent. Amyloid degeneration often 
supervenes upon this form of nephritis. 



214 DISEASES OF THE URINARY SYSTEM. 

Symptoms. — While similar to the acute form, this variety is 
much more insidious in its development. 

1. Anemia is more marked than in the acute form, is of a 
progressive character, and is associated with weakness and 
emaciation. 

2. Dropsy is also prominent, appearing first about the eyes, 
and then becoming general. 

3. Gastro-intestinal derangements are common. 

4. Uremia is less frequent than in the acute form. 

5. Thoracic complications often occur; they include bron- 
chitis, pneumonia, pulmonary edema, pleurisy, and peri- and 
endocarditis. 

6. Urinary changes. 

a. Quantity and specific gravity about normal, but 
varying. 

b. Color pale; whitish sediment common. 

c. Albumin present in large amount (1-5%). 

d. Urea diminished. 

e. Casts: broad; finely granular, fatty and hyaline. 

/. Blood corpuscles, if present, suggest an intercurrent 

acute nephritis. 
Should contraction occur, the urine approximates in char- 
acter that of chronic interstitial nephritis. 
Diagnosis is usually easy, the urinary changes, together with 
the marked dropsy and anemia, distinguishing this from 
the interstitial form. The amyloid variety can be recognized 
only in connection with a history of suppuration and the pres- 
ence of amyloid changes in other organs. 

Prognosis. — Generally unfavorable, death occurring within 
two years. Careful treatment may, however, partially arrest 
the disease; and should contraction occur there may appear 
to be a practical restoration to health. 

Treatment. — 1. Until the symptoms abate, treat as an acute 
case. Then allow a mixed diet, limiting it again if active 
symptoms or gastro-intestinal irritation appear. 



DISEASES OF THE URINARY SYSTEM. 215 

2. Hot baths given daily at bedtime are of great benefit. 

3. Keep the bowels relaxed. 

4. Administer pure, preferably distilled, water freely. 

5. Avoid chill; let the patient wear woolen under- 
clothing and if necessary remove him to a warm, moist 
climate in winter. 

6. Uremia, dropsy, and anemia should be treated symptom- 
atically as in the acute form. 

7. Medicines. Cantharis is frequently indicated by scanty, 
highly albuminous urine associated with dropsy, even though 
other symptoms be lacking. Mercurius corros. has less effect 
upon dropsy, but is well suited to cases in which dropsy and 
other acute symptoms have subsided but the urine remains 
albuminous and rather scanty. Anemia, gastro-intestinal irri- 
tation, and a history of syphilis further indicate it. The latter 
may also suggest the use of kaliiod. or aurmn. Dropsy with a 
tendency to uremic symptoms calls for the use of cuprum 
ars. 

CHRONIC INTERSTITIAL NEPHRITIS. 

(Red Granular, Contracted, or Gouty Kidney.) 

Etiology. — The causes, while often obscure, include: 

1. Gout. The uric acid diathesis may be associated with 
alcoholism. 

2. Lead. Chronic plumbism induces gouty changes. 

3. Prolonged passive congestion, the result of heart disease. 

Heredity, infectious diseases (scarlatina, malaria, rheuma- 
tism, syphilis) and digestive disorders have some causative 
influence. It occurs in middle life, and is usually associated 
with sclerosis of other organs; and it is a constant feature of 
old age. 

Pathology. — The disease is essentially a connective tissue 
hyperplasia which destroys the tubules by compression. The 



216 DISEASES OF THE URINARY SYSTEM. 

kidney is small, red, and granular, with a greatly atrophied 
cortex and an adherent capsule. Microscopically, great bands of 
intertubular connective tissue are seen; by this contraction the 
tubules are in part obliterated, leaving dilated portions (cysts). 
General arterio-sclerosis, with hypertrophy of the heart, is 
invariably associated. 

Symptoms. — The disease is extremely insidious ; there may be: 

1. Slight gradual loss of strength, with digestive disturb- 
ances. 

2. Cardio-vascular changes : 

a. Rigid arteries with a high tension pulse. 

b. Hypertrophy of the left ventricle, with a sharp accent- 
uation of the second sound at the aortic orifice. 

3. Slight edema, under the eyes or about the ankles. 

4. Urinary changes. The urine is increased in quantity, 
pale, of low specific gravity (1003-1015), and the excretion 
of urea is diminished. There may or may not be a small 
amount of albumin ; and casts, mostly hyaline, are usually 
present. 

The patient commonly has to arise at night to micturate; 
and should this or some other symptom lead to examination 
of the urine, the disease is easily recognizable. Many cases, 
however, remain unsuspected until the onset of: 

5. Uremia (headache, vertigo, drowsiness, coma, convul- 
sions, etc.). 

6. Dimness of vision (albuminuric retinitis). 

7. Hemorrhage, cerebral or elsewhere. 

8. Dilatation of the heart, with dropsy, a diminished 
quantity of urine, dyspnea, and reduplication of the first 
sound, may occur in the later stages. 

Diagnosis. — Examination of the urine usually insures discovery 
of the disease. 

Passive renal hyperemia, the result of uncompensated heart 
disease, may be distinguished by the history of the primary 



DISEASES OF THE URINARY SYSTEM. 217 

disease, the less marked arterio-sclerosis, and the fact that 
urea is little diminished and the urine contains only a few 
small hyaline casts; the condition usually disappears upon the 
restoration of cardiac compensation. 

Chronic parenchymatous nephritis is accompanied by marked 
dropsy, occurs earlier in life, presents little cardio-vascular 
change, and the urine is highly albuminous with broad granu- 
lar and hyaline casts. 

Prognosis. — While the damage is irremediable, the process 
may be checked; and if sufficient renal parenchyma remains 
intact, life may be prolonged indefinitely. Persistent diminu- 
tion of urea (below 175 grains per day) or actual uremic 
symptoms render the outlook unfavorable. 

Treatment. — 1. Arrest the change in the blood vessels. This 
is possible if gout be the cause, the treatment being dietetic 
(restriction as to nitrogenous foods, etc.), and hygienic (main- 
tenance of body warmth by clothing or climate; fresh air, 
moderate exercise and avoidance of excitement). 

2. Control symptoms as they arise. Such complications as 
bronchitis, pneumonia and pleurisy must be treated symptom- 
atically; and the management of uremia has been considered 
elsewhere. 

3. Medicines. Chloride of gold, 2x in a fresh watery solu- 
tion, is of great value in the early stages, especially when 
various neurotic symptoms are present. Rhus tox. possesses 
a decided eliminative value, and is frequently indicated by 
gouty symptoms. Plumbum, which offers a perfect simile 
to the conditions present, is frequently suggested by digestive 
and abdominal symptoms. Mercurius corr. is suited to 
intercurrent acute or subacute exacerbations, and to syphilitic 
cases. Glonoin is invaluable when the high arterial tension 
occasions throbbing headache, etc. Phosphoric acid (general 
neurasthenic symptoms with excessive urination), nux vomica 
(digestive disorders) and arsenic (thirst, debility, and urinary 
symptoms) are frequently useful. 



218 DISEASES OF THE URINARY SYSTEM. 



AMYLOID KIDNEY. 

Etiology. — Lardaceous degeneration of the kidney is a se- 
quence of prolonged suppuration or cachexia (bone disease, 
tuberculosis, syphilis). 

Pathology. — Waxy infiltration begins in the capillaries of the 
malpighian tufts, involves blood vessels and tubules, and is 
associated with diffuse nephritis. The kidney becomes large, 
smooth, anemic, and "bacon-like" on section, the degener- 
ated areas staining a mahogany-brown on the application of 
an iodine solution. 

Symptoms. — The general symptoms of chronic parenchy- 
matous nephritis are added to those of the causative disease, 
and in addition amyloid changes may be detected in the liver, 
spleen and often the intestines. Dropsy is moderate. The 
urine is pale, copious, of low specific gravity (1005-1015) 
and highly albuminous, with a moderate number of hyaline 
or waxy casts. 

Diagnosis. — The history and the discovery of simultaneous 
enlargement of the liver and spleen are necessary for positive 
diagnosis. Parenchymatous nephritis lacks the causative 
factors and presents more general dropsy; but the two forms 
are often associated. Interstitial nephritis has little dropsy, 
slight albuminuria, and scanty urinary sediment. 

Prognosis.— Recovery is impossible, but occasionally control 
of the causative may check the renal degeneration. 

Treatment must be directed toward the primary disease, 
while the kidney lesion should receive the attention recom- 
mended for the other forms of nephritis. 



DISEASES OF THE URINARY SYSTEM. 219 

PYELONEPHRITIS. 

("Surgical Kidney;" Suppurative Interstitial, Obstructive, or Ascending 

Nephritis. ) 

Etiology. — The kidney may become infected by pyogenic 
organisms through: 

1. The genito-urinary tract, as the result of the inflamma- 
tion attendant upon the passage of calculi or even uric acid 
"sand," as the sequence of unclean surgical interference, or 
by extension upward of a ureteritis, cystitis, or urethritis. 

2. The blood-vessels, e. g. y by septic emboli, in connection 
with pyemia, etc. 

3. Renal affections, such as tuberculosis, carcinoma, etc. 

4. Toxic irritants (cantharis, copaiba, and other irritants 
given as diuretics, etc.). 

5. Traumatism (penetrating wounds involving the kidney) 
and extension of neighboring abscesses. 

Pathology.— The suppuration, usually advancing from below, 
first involves the renal pelvis {pyelitis) and then the substance 
of the kidney itself. Foci of suppuration may develop in one 
or both kidneys, forming multiple abscesses which later unite 
and finally burst into the pelvis of the kidney, whence the pus 
is discharged with the urine. In advanced cases the kidney 
may be simply a collection of purulent sacs or one large 
abscess. Distention of the renal pelvis and calyces with pus 
{pyonephrosis) may result from partial obstruction of the 
ureters. 

Symptoms — The early symptoms are indefinite. When the 
suppurative process remains confined to the renal pelvis {pye- 
litis), the clinical manifestions may be limited to slight fever, 
some tenderness in the region of the kidney, and small amounts 
of pus and mucus in the acid, slightly albuminous urine. With 
extensive involvement of the renal parenchyma, however, 
there is apt to be: 

1. Aching or pain in the region of the kidney. 



220 DISEASES OF THE URINARY SYSTEM. 

2. Rigors, sweats, and a septic temperature range. 

3. Rapid emaciation, gastric irritability, and a typhoid state. 

4. The urine becomes diminished in quantity, of low specific 
gravity, and albuminous. It contains pus, blood, bacteria, 
and perhaps casts. The amount of albumin is in direct pro- 
portion to the quantity of pus and blood present. The excre- 
tion of urea is diminished. 

Diagnosis. — In many cases the renal lesion is masked by the 
symptoms of the primary disease (cystitis, nephrolithiasis, 
etc.). Repeated examinations and urinalyses maybe neces- 
sary before a diagnosis is possible; and the latter usually rests 
upon the discovery, in connection with possible causes and 
vague symptoms, of pus, blood, and perhaps caudate epithelial 
cells from the pelvis of the kidney in the urine. 

Prognosis. — In all but the mildest cases of pyelitis, the prog- 
nosis is extremely unfavorable. Life may be prolonged, how- 
ever, and if the cause (e. g., obstruction of the ureter) is 
removable, recovery is possible. 

Treatment. — The physician should endeavor, by prompt at- 
tention to urethral and cystic inflammations, and by cleanli- 
ness in all instrumentation about the genito-urinary tract, to 
guard against the possibility of renal infection. Upon the 
appearance of any symptoms suggesting the existence of 
pyelitis or pyelonephritis, the patient should be placed at rest, 
hot fomentations applied, and his diet restricted to milk and 
other bland liquids. A medicine having a local antiseptic 
action on the kidney should be given: cystogen, or urotropin, 
gr. v. t. i. d., saccharin, gr. ij. t. i. d., or metliylene blue, gr. j. 
in caps. t. i. d. The suppurative process affords indications 
for such remedies as mercur. corr. or hepar ; the renal changes 
may be met by the administration of terebinth, cuprum arsen., 
or cantharis ; and general septic conditions sometimes afford 
indications for arsenic, carbolic acid, baptisia, or lachesis. 



DISEASES OF THE URINARY SYSTEM. 221 



TUBERCULOSIS OF THE KIDNEY. 

Etiology. — Renal tuberculosis may develop — 

1. In connection with acute general tuberculosis. 

2. In connection with tuberculosis elsewhere in the genito- 
urinary tract. Tuberculosis of the epididymis, seminal vesi- 
cles, prostate, or bladder usually pre-exists. Often it affects 
adolescent males after gonorrhea, especially if the latter has 
been complicated with epididymitis; and in these cases it 
involves the ureter first, thence ascending to the pelvis and 
finally involving the parenchyma of the kidney. 

3. Primary renal tuberculosis is rare. Usually it is unilat- 
eral. 

Pathology. — 1. In connection with general tuberculosis, mil- 
iary tubercles may develop in the kidney, but they occasion 
no special symptoms. 

2. Tuberculosis ascending from the lower portions of the 
tract is apt to be double. It occasions pyonephrosis or renal 
or peri-renal abscess, frequently followed by septicemia. 

3. Primary renal tuberculosis occurs as an infiltration of the 
parenchyma; the areas undergo caseation and softening, the 
organ becoming honey-combed with cavities, and the pus 
is discharged through the ureter. 

Symptoms. — The symptoms are vague at first; there may be 
pus or blood in the urine, evening pyrexia, some tenderness 
or pain in the loin, and in general the signs of pyelonephritis. 
The diagnosis rests upon: 

1. The discovery of tuberculosis elsewhere. 

2. The absence of any cause for pyelonephritis. 

3. The discovery of tubercle bacilli in the urine. 
Prognosis. — Unfavorable. 

Treatment. — An early diagnosis, which can be assured only 
by the repeated examination of ever} 7 pus-containing urine for 
the tubercle bacillus, should be followed by an immediate 
nephrotomy. 



222 DISEASES OF THE URINARY SYSTEM. 

NEPHROLITHIASIS. 

(Renal Calculus; Stone in the Kidney.) 

Etiology. — The urinary solids are precipitated about a nucleus, 
often of epithelial cells, mucus, or blood clot, to form a con- 
cretion. 

Varieties. — 1. Uric acid (smooth, firm, brown, or black; often 
multiple). 

2. Oxalate of lime (uneven, hard, and brown; "mulberry 
calculus"). 

3. Phosphates (large, soft, and white). 

4. Cystin and xanthin (rare). 

Course. — 1. The stone may remain quiescent in the kidney 
tubules or substance, growing to a considerable size and occa- 
sioning vague symptoms until it has bored out for itself a 
pocket — a so-called "nesting stone." It may enter the pelvis, 
where it grows and often assumes the shape of that cavity. 

2. The stone may pass down the ureter, with or without 
renal colic. 

3. The stone may become impacted in the ureter, blocking 
the out-flow of urine and causing hydro- or pyonephrosis, sup- 
pression, or abscess. 

4. The stone may break into the retroperitoneum or the 
peritoneal cavity from either the kidney or the ureter. 

Symptoms. — The symptoms vary according to the situation 
and course of the stone. 

1. The existence of a stone in the kidney causes few symp- 
toms unless it is free in the pelvis or entering the ureter. 
Under these circumstances it causes: 

(a) Pain, which may be direct, varying from mere uneasi- 
ness to severe paroxysmal or continuous pain in the region of 
the kidney, associated with tenderness and rigidity, and 
aggravated by motion; or reflex, extending to the groin, 



DISEASES OF THE URINARY SYSTEM. 223 

testicle, and inner side of the thigh, along the course of the 
genito-crural nerve, or along the line of the ureter. 

(ft) Hematuria, irregular in its occurrence but always in- 
creased fty exercise. The blood may appear clear or smoky in 
the urine, or it may occur in the form of worm-like clots. 

(c) Cystic symptoms may alone be present, micturition be- 
ing frequent and the urine containing pus and crystals. 

(d) Digestive disturbances, vague in character, may accom- 
pany the renal disease. 

2. Passage of the stone down the ureter is usually accom- 
panied by renal colic. At the moment when the stone enters 
the ureter the patient is suddenly seized with agonizing pain 
in the loin which radiates down the line of the ureter into the 
root of the penis, the prostate, the scrotum, or the thigh. 
The terrific pain may compel the patient to writhe, rolling on 
the floor, and bending double in order to relax the ileo-psoas 
and lumbar muscles; and symptoms of shock and even col- 
lapse, with cold sweat, sometimes ensue. Vesical irritation, 
tenesmus, constipation, and vomiting frequently accompany 
the paroxysm. At times the symptoms strongly suggest in- 
testinal obstruction. After a period varying from minutes to 
hours the pain ceases as suddenly as it began, owing to the 
passage or recession of the stone. Subsequently the urine 
may contain pus or blood. 

3. Impaction of the stone in the ureter leads to recurrences 
or persistence of the colic, and, as a rule, distinct localized 
pain and tenderness may be located near the entrance to the 
bladder by rectal or vaginal palpation. The ureteral orifice is 
exquisitely tender, and if obstruction is incomplete, blood, 
pus, and crystals appear in the urine. 

Diagnosis. — Stone in the kidney must be distinguished from 
renal tuberculosis ; in the latter the patient's physique and 
family history, the usual absence of renal colic, the lack of 
benefit from rest or aggravation from motion, and the appear- 
ance of little blood and no crystals in the urine will generally 



224 DISEASES OF THE URINARY SYSTEM. 

suffice for diagnosis. Discovery of the tubercle bacillus in the 
urinary sediment is conclusive. 

Biliary colic is accompanied by pain radiating from the 
right hypochondrium into the umbilicus, into the right shoulder- 
tip and the angle of the scapula, with tenderness over the gall 
bladder or the Mayo-Robson point. Jaundice is common, and 
urinary symptoms and signs are absent. 

Prognosis. — Because of the possible complications the progno- 
sis must be guarded. Renal colic is rarely fatal in itself. 

Treatment. — Attacks of renal colic may be palliated by the 
application of hot fomentations, or better, a long-continued 
hot general bath. Frequently the hypodermatic use of 
morphia, gr. %, with atropia, gr. y-jhr, is necessary. Bella- 
donna, bcrberis, and mix vomica are medicines frequently 
indicated. 

In the interval between attacks, the diathetic state requires 
careful attention. In a majority of cases the patient is gouty, 
and the therapeutic measures must be directed to that condi- 
tion. Meats, eggs, alcoholics, etc., should be forbidden, and 
pure or alkaline water prescribed in large quantities. If, how- 
ever, there is phosphaturia and alkaline urine, forbid an ex- 
cess of vegetables and milk, allow meats, and administer dilute 
hydrochloric acid to acidulate the urine. The more important 
remedies are calcarea, lycopodium, sarsaparilla, and sulphur. 

In painful and persistent cases it is advisable to explore the 
kidney with nephrolithotomy, evacuation of abscesses, sound- 
ing or flushing the ureter, etc. The kidney can be opened 
from end to end, explored, and drained or sutured with im- 
punity. (Van Lennep.) 



HYDRONEPHROSIS. 

Etiology. — The renal pelvis becomes distended with retained 
watery secretion as the result of gradually developed obstruc- 
tion to the outflow, sudden complete obstruction leading 



DISEASES OF THE URINARY SYSTEM. 225 

simply to absolute suppression of urine. This gradual ob- 
struction may be due to — 

1. Impaction of a calculus in the ureter. 

2. Stricture of the ureter (congenital or inflammatory). 

3. Twisting of the ureter (floating kidney). 

4. Pressure upon the ureter by inflammations, tumors, 
cicatrices, etc., from without. 

5. Obstruction in or below the bladder (tumors, enlarged 
prostate, urethral stricture), which tends to cause bilateral 
hydronephrosis. 

Pathology. — The pressure of the retained fluid causes — 

1. Distention of the pelvis of the kidney. 

2. Pressure-atrophy of the kidney tissue, which finally 
leaves nothing but a thin-walled cyst. Infection renders the 
condition one of pyonephrosis. 

Symptoms. — 1. A fluctuating tumor develops in the region of 
the kidney and enlarges downward and forward toward the 
groin, following the line of the ureter. 

2. An excessive flow of urine, followed by a notable dimi- 
nution in the size of the tumor, ma}' be observed occasionally 
{intermittent hydronephrosis). This symptom is inconstant, 
however; as a rule, it occurs in those cases due to twisting of 
the ureter by a movable kidney. 

3. No subjective symptoms are occasioned by slight disten- 
tion, but as the tumor increases, pressure symptoms, such as a 
tense feeling in the abdomen, nausea, vomiting, and constipa- 
tion, may appear. 

4. The urine is normal in quantity, except in the rare cases 
of double hydronephrosis, and is free from albumin. Double 
hydronephrosis quickly leads to anuria, uremia, and death. 

Diagnosis.- — This rests upon discovery of the tumor in the 
flank, its enlargement in the characteristic direction, the ex- 
clusion of other abdominal tumors, and in doubtful cases 
examination of the aspirated fluid, which resembles weak 
urine and contains urea and uric acid. 
15 



226 DISEASES OF THE URINARY SYSTEM. 

Treatment. — When the obstruction is due to a stone, the loin 
may be massaged and the bladder distended in an attempt to 
overcome the block. Aspiration may be made repeatedly, 
but when it fails to afford permanent relief it is wise to incise 
and drain the sac, and to remove or overcome the ureteral 
obstruction by operative means if possible, or to extirpate the 
kidney if the latter is extensively diseased. 



FLOATING OR MOVABLE KIDNEY. 

Etiology. — As a result of relaxation of its surrounding tissues, 
one kidney, usually the right, becomes displaced and may be 
found as a movable tumor in any part of the abdomen. Pre- 
disposition is found in : 

1. Women, six times as often as men, because of — 

a. Relaxation of the abdominal walls. 

b. Relaxation of the peritoneum. 

c. Repeated pregnancies. 

d. Tight lacing. 

2. Middle life. Rarely it may be congenital. 

3. Muscular exertion, such as heavy lifting. 

Mobility of the kidney is frequently associated with a down- 
ward displacement of all the abdominal viscera {splanchnop- 
tosis}. 

Symptoms. — 1. Subjective sensations may be slight or want- 
ing; often they are limited to vague "dragging" pain. 

2. Reflex nervous symptoms are sometimes marked; they 
consist of flatulence, palpitation, neuralgic pain in thorax or 
abdomen, irritable bladder, dysmenorrhea, and the train of 
symptoms commonly attributed to uterine disease. 

3. Twisting of the ureter, involving vessels and nerves, may 
occasion the agonizing pain and other symptoms of renal 
colic, and may lead to hydronephrosis. 

Diagnosis. — Bimanual palpation, with the patient in various 



DISEASES OF THE URINARY SYSTEM. 227 

positions if necessary, reveals a smooth reniform tumor, which 
is freely movable; and pressure develops a peculiar sickening 
pain. 

A distended gall-bladder forms a fluctuating pyriform cyst, 
non-separable from the liver, which is totally unlike the firm 
kidney. On pressure a movable kidney frequently becomes 
lost in the abdomen, while the gall-bladder springs back to its 
previous position when that pressure is removed. Other ab- 
dominal tumors are more painful, have not the shape or 
peculiar tenderness of the kidney, are apt to have an uneven 
surface, and if malignant in nature they are apt to be asso- 
ciated with cachexia. 

Treatment. — Many cases require no treatment. If the symp- 
toms become annoying, rest on the back followed by applica- 
tion of a binder and pad or truss may suffice to retain the 
kidney in place. Should this prove ineffective, the kidney 
may be stitched in its normal position (nephrorrhaphy), or 
better, a plastic union may be secured (nephropexy). 

CYSTITIS. 

Etiology. — Inflammation of the bladder results from local 
microbic infection, due to: 

1. Irritants within the bladder (calculi, foreign bodies, etc.). 

2. Obstruction to micturition (stricture, prostatic hyper- 
trophy) with resulting decomposition of the retained urine. 

3. Extension of inflammation from without (gonorrhoea, 
etc.). 

4. Toxic substances (cantharides, capsicum, etc.). 

5. Traumatism (direct injury to the bladder, etc.). 
Pathology. — The mucous membrane is inflamed, perhaps 

ulcerated or denuded, and in chronic cases it may be thick- 
ened; mucus, pus, and epithelium are discharged in large 
quantities. 

Symptoms. — The disease may be acute (febrile) or chronic; 
it is accompanied hy-- 



228 DISEASES OF THE URINARY SYSTEM. 

1. Frequent and painful micturition. 

2. Tenderness or pain over the bladder. 

3. Urine which contains pus and mucus (hence it is glairy), 
together with epithelial cells and sometimes blood. 

Diagnosis. — Pyuria with vesical pain and tenesmus is pathogno- 
monic of cystitis. Chronic interstitial nephritis, possibly co- 
existing, is indicated by the presence of casts in the urine and 
by the associated signs of cardio-vascular sclerosis. Pyelitis 
or pyelo nephritis can often be excluded with difficulty or not 
at all. 

Prognosis. — In acute cases the prognosis is usually good; in 
chronic cases the outlook is less favorable, but recovery is 
possible if the cause can be removed. 

Treatment. — The patient should be placed at absolute rest in 
bed, pure water should be administered freely, and a plain, pref- 
erably milk, diet must be given until active symptoms sub- 
side. The cause should be sought out and treated. Boric 
acid, five grains every four hours, or cystogen, gr. v t. i. d., 
should be administered in order to render the urine aseptic. 

Aconite and gelsemium are indicated early in acute cases. 
Later, and in chronic cases, belladonna, cantharis, and mer- 
curius corrosivus are often useful. Terebinth is a remedy of 
great value, particularly in cases attended with intense irri- 
tability of the bladder. 

Cases dependent on obstruction demand catheterization, at 
times antiseptic irrigation; and occasionally incision and drain- 
age becomes necessary. 

INCONTINENCE OF URINE. 

Etiology. — Incontinence of urine (enuresis) may be — 

1. Paralytic (spinal lesions involving sphincteric centre). 

2. Irritative (calculus, cystitis, parasites, etc.). 

3. Mechanical (retention with over-distention; pressure 
from without, as of the fetal head during labor). 



DISEASES OF THE URINARY SYSTEM. 229 

4. Spasmodic (overaction of compressor muscle, with di- 
minished vesical capacity). 

Treatment varies according to the cause. The nocturnal 
enuresis of children may be due to any of these conditions, 
and it is particularly necessary to exclude epilepsy and local 
irritations due to ascarides, elongated prepuce, or masturba- 
tion, before deciding the symptom to be purely neurotic. In 
a case of the latter class the bowels should be kept open, 
the evening meal must be light, and the bladder must be 
emptied at bedtime. This, with the administration of such 
remedies as belladonna, equisetum, or sulphur, will usually 
affect a cure. 

Retention of urine may be neurotic (hysteria) or mechanical 
(obstructive) in origin. The latter may be due to stricture, 
enlarged prostate, impacted calculus, or pressure upon the 
urethra by tumor or gravid uterus. It is sometimes the only 
symptom of commencing peritonitis in women. 

Suppression of urine is due to secretory failure of the kidney 
and the resulting symptoms are those of uremia. 



DISEASES OF THE DIGESTIVE 

TRACT. 



AFFECTIONS OF THE MOUTH AND THROAT. 

It is a time-honored custom to begin the examination of a 
patient by inspecting his tongue, and if the other structures 
about the mouth, the lips, teeth, gums, fauces and pharynx, 
are included in the inspection, much of diagnostic importance 
can thus be elicited. 

The patient should face a good light, or if the latter is arti- 
ficial it should be reflected into the mouth. The examiner 
should first inspect the lips, noting their color — blue in cyan- 
osis, pale in anemia, dry and often brown in fevers — and the 
presence of any fissures or ulcers or of herpes. Then notice 
the teeth, whether they are moist, or dry and covered with 
sordes; whether they are decayed or many missing, this tend- 
ing to bring about various digestive and other disturbances; 
and if the patient is a child, whether the proper number of 
teeth have appeared, and whether they are notched (hereditary 
syphilis). Note the color of the gums, and whether they are 
spongy and soft, indicating scurvy. Look for the blue line 
near the insertion of the teeth which indicates lead poisoning. 

Then have the patient protrude his tongue, and note whether 
he puts it out in a straight line — deviation indicates unilateral 
palsy. Notice whether it is tremulous, as in fevers and ex- 
haustions. Note its color. It should be red and moist. The 
coated tongue of gastric disorder, the reddened tongue of 
fever, the brown, fissured tongue of the typhoid state, the 
strawberry tongue of scarlet fever, and the pigmented tongue 
of Addison's disease should be noted. The fissured tongue 
suggests kidney disease; the dry tongue, lack of digestive 



232 DISEASES OF THE DIGESTIVE SYSTEM. 

activity. Note any ulcers or marks of the teeth upon the 
tongue. 

Introducing a tongue depressor, note the color and general 
appearance of the soft palate, fauces, and pharynx. Note the 
presence of any ulcers or mucous patches. Determine whether 
the tonsils are enlarged, and whether there is any exudate 
upon them; and if there is, ascertain the condition of the 
underlying surface. (Notice whether the exudate appears 
upon the pillars of the fauces or the uvula.) 

Inspect the pharynx. Note if it be markedly granular, if 
enlarged follicles are present, if there is an excess of mucus or 
any ulceration. 

If the breath be bad, note whether the foul odor comes from 
the nose or the mouth, having the patient breathe through 
each in turn. If both are bad, the odor may come from the 
lungs, and will be increased by having the patient cough. It 
may be uremic (urinous odor), diabetic (sweetish), or simply 
the result of digestive disorder. 



STOMATITIS. 

Etiology. — Inflammation of the mouth is excited by local 
irritation, which may be mechanical (e. g. t injury from a 
sharp tooth), chemical (drugs and beverages), thermal (hot 
or cold food), or parasitic. Among the predisposing causes 
are cachectic states and gastro-intestinal diseases. Stomatitis 
occurs principally in young children. 

Symptoms. — The patient suffers with pain and heat in the 
mouth, accompanied with an increased secretion of saliva, 
fetid breath, and fever. A young child becomes restless, and 
is disinclined to nurse. 

Varieties. — 1. Simple stomatitis. Diffuse redness and swell- 
ing of the mucous membrane; no ulceration. 

2. Aphthous stomatitis (herpetic, vesicular). Vesicular 
spots which break down and become small ulcers. 



DISEASES OF THE DIGESTIVE SYSTEM. 233 

3. Ulcerative stomatitis. Inflammation along the border 
of the gums which becomes ulcerative. 

4. Membranous stomatitis. Catarrhal inflammation fol- 
lowed by the appearance of a pseudo-membrane, which be- 
comes disintegrated and cast off, leaving an ulcerated surface. 
This may be a diphtheritic extension or the effect of a cor- 
rosive poison. 

5. Gangrenous stomatitis (noma; cancrum oris). A small 
blister appears inside the cheek and extends rapidly, with 
induration, sloughing, and extensive tissue destruction. 

6. Mycotic stomatitis (thrush). A fungus (saccharomyces 
albicans) appears in numerous milk white elevations, which 
leave a raw, bleeding surface when detached. 

7. Bednar s aphtha. Attacks only infants under six weeks 
of age. Small superficial ulcers on the palate, due to trau- 
matism (nipple). 

Prognosis. — Bad in the gangrenous form, grave in the mem- 
branous, guarded in the ulcerative, and in the other varieties 
favorable. 

Treatment. — Secure cleanliness of the mouth \>y swabbing 
with boric acid solutions. In the gangrenous form the lesion 
must be thoroughly cauterized, antiseptics being used there- 
after. Among the more important remedies are argent, nitr., 
borax , hepar, kali chlor., merenrius, nitric acid, and sulphur. 



GLOSSITIS. 

Etiology. — Inflammation of the tongue may be superficial or 
parenchymatous, acute or chronic. It may result from trau- 
matism, toxic irritants, such as tobacco fumes, acids, etc., and 
occasionally it is symptomatic of digestive inflammations and 
infectious fevers. 

Symptoms. — The superficial variety is accompanied by slight 
stiffness, soreness, and pain when the tongue is moved. The 
parenchymatous inflammation is, fortunately, rare; the tongue 



234 DISEASES OF THE DIGESTIVE SYSTEM. 

becomes enormously swollen and may finally suppurate, acute 
pain and serious interference with respiration accompany it, 
and fever and other constitutional symptoms may be severe. 

Prognosis. — The superficial form recovers quickly, but the 
parenchymatous variety is severe, often fatal, and at best is 
apt to lead to permanent deformity of the tongue. 

Treatment. — The superficial form requires only local cleanli- 
ness to bring about recovery. The parenchymatous form may 
demand longitudinal incision of the tongue, even before sup- 
puration, and often tracheotomy is necessary. Early in the 
attack belladonna is usually indicated, but the involvement of 
the deeper structures will require the use of such drugs as 
mercury, lachesis, rJius tox., and hepar. Edema may suggest 
apis and in the stage of resolution the iodides and sulphur are 
useful. The mouth should be cleansed with solutions of boric 
acid, listerine, or some similar preparation. 



ACUTE TONSILLITIS. 

Etiology. — The exciting cause is probably an infective agent, 
the predisposing factors including — 

1. Exposure to cold and wet. 

2. Diathetic states, especially gout. 

3. Acute infectious disease (measles, scarlatina, rheuma- 
tism). 

4. Youth or adolescence. 

Pathology. — According to the extent of the lesions three 
varieties are recognized, viz. : 

1. Acute catarrhal tonsillitis, in which the inflammation is 
limited to the mucous membrane covering the tonsil, the 
latter appearing swollen and congested. 

2. Acute follicular tonsillitis, in which the inflammatory 
process leads to desquamation of the epithelium and the latter 
collects in the crypts of the tonsil as small, whitish, cheesy 
masses. 



DISEASES OF THE DIGESTIVE SYSTEM. 235 

3. Acute suppurative tonsillitis (phlegmonous tonsillitis, 
quinsy) in which the glandular structure becomes inflamed 
and undergoes suppuration. 

Symptoms. — The onset is usually sudden and is marked by 
sore throat, moderate fever, and the usual febrile symptoms 
{headache, backache, na?isea or vomiting, etc.). The swelling 
of the tonsils may cause distress on deglutition, and in some 
cases edema of the palate and pharynx leads to dysphagia and 
even serious dyspnea. 

Diagnosis. — As a rule, inspection of the throat suffices for 
diagnosis. In diphtheria the exudate when stripped off shows 
a raw surface beneath, the exudate usually extends to the 
fauces or uvula, and doubt can be removed by examination of 
a culture for the Klebs-Loeffier bacillus. 

Prognosis. — Favorable. Recovery within a week is the rule. 

Treatment. — If there is much inflammation cold should be 
applied externally and the patient given bits of ice to suck. 
The catarrhal form yields quickly to guaiacum. The more se- 
vere cases frequently present indications for aconite, belladonna, 
or Phytolacca at the outset. Following this, mercur. biniod. 
or rhus tox. may be required, or the tendency to suppuration 
may suggest baryta carb. or hepar. When pus can be made 
out, puncture the abscess with a sharp-pointed bistoury 
wrapped to within one-half inch of its point with adhesive 
plaster. In the intervals between recurring attacks, attention 
should be directed to the discovery and treatment of any 
diathetic state. 



HYPERTROPHY OF THE TONSILS. 

Etiology. — Chronic enlargement of the tonsils is particularly 
common in children, owing to strumous conditions, recurrent 
attacks of acute tonsillitis, or involvement of the tonsils in 
connection with the acute infectious diseases. It is often 
associated with adenoid overgrowths at the vault of the 
pharynx. 



236 DISEASES OF THE DIGESTIVE SYSTEM. 

Pathology. — The lymphoid elements may be multiplied, the 
gland being- enlarged but soft; or the fibrous tissues maybe 
increased, rendering it firm in consistence. 

Symptoms. — The majority of the symptoms are the result of 
mechanical interference with respiration; they include mouth- 
breathing, snoring, disturbed rest, and even attacks of 
dyspnea. The voice is thick and nasal, and hearing may be- 
come impaired through implication of the eustachian tube and 
middle ear. As the result of deficient aeration of the blood, 
general nutrition is poor, the patient is pale and anemic, his 
face takes on a vacant expression, and the chest may become 
actually deformed into a "chicken breast." 

Diagnosis. — By examination of the throat. Palpate the tonsil 
to decide whether the hypertrophy is fibrous. 

Prognosis. — While the hypertrophy tends to disappear about 
the time of puberty, much damage to the child's development 
may have been done by that time. The prognosis as to the 
latter depends, therefore, upon the time of removal of the 
cause. 

Treatment. — If the tonsil is hard and fibrous, tonsillotomy is 
advisable; but if the tissues are soft improvement can often be 
secured by the persistent administration of mercur. biniod., or 
the iodides of iron, lime, sulphur, etc. 



ACUTE CATARRHAL PHARYNGITIS. 

(Acute Sore Throat.) 

Etiology. — Acute inflammation of the mucous membrane of 
the pharynx occurs, especially in children, as the result of 
exposure to cold and wet. Diathetic states predispose to it. 

Symptoms. — The throat becomes raw and sore and there is 
pain on swallowing, with a constant inclination to clear the 
throat. Extension to the eustachian tube may produce partial 
deafness, or involvement of the larynx may cause hoarseness. 
Examination shows the pharynx to be red and often covered 
with mucus. 



DISEASES OF THE DIGESTIVE SYSTEM. 237 

Treatment. — Gargles of hot water, inhalations of steam, ap- 
plications of pure glycerine or astringents, and sprays of 
albolene are useful aids in relieving the sore throat. The 
more important internal medicines are aconite, belladonna, 
giiai acnm, and Phytolacca; occasionally indications exist for 
apis (edema), lachesis (hyperesthesia), etc. 



CHRONIC PHARYNGITIS. 

Etiology. — Chronic pharyngitis usually occurs in adults as the 
result of repeated acute attacks, of the use of alcohol or 
tobacco, of long-continued nasal catarrh, or of over-use of the 
voice. 

Varieties. — 1. Hypertrophic pharyngitis (granular or folli- 
cular), in which the mucous membrane is congested, thickened, 
traversed by dilated blood vessels, and studded with the 
"split-pea" elevations of distended follicles. 

2. Atropine pharyngitis (pharyngitis sicca) in which the 
mucous membrane is pale and dry, while secretion is scanty. 

3. Ulcerative pharyngitis. Ulceration of the pharynx may 
be due to syphilis, tuberculosis, diphtheria, simple inflamma- 
tion, or lowered nutrition. That due to tuberculosis is pain- 
ful, while the syphilitic is painless and may be associated with 
mucous patches. 

4. Phlegmonous pharyngitis ^ i. e., suppuration involving 
the pharynx, may be due to extension of a tonsillitis, to acute 
infection of the pharynx itself, or to injuries, scalds, or cor- 
rosive poisons. 

Symptoms. — In all these varieties there are sore throat, weak 
or husky voice, and disagreeable sensations of fulness, tickling, 
or even pain. The phlegmonous form is attended with high 
fever, difficult deglutition, and rapid prostration, and may end 
fatally. 

Treatment. — This is usually directed to the discovery and re- 
moval of the cause. Enlarged follicles are removed by the 
galvano-cautery, ulcers are treated with silver nitrate and 



238 DISEASES OF THE DIGESTIVE SYSTEM. 

antiseptics, and constitutional states, such as those associated 
with tuberculosis or syphilis, receive appropriate treatment. 



RETROPHARYNGEAL ACSCESS. 

Retropharyngeal abscess, a suppurative process occurring in 
the connective tissue between the pharynx and the vertebral 
column, is the result of caries of the vertebrae, tubercular or 
syphilitic, of naso-pharyngeal disease, of the acute infections, 
or of faulty nutrition. It is accompanied by pain, swelling, 
interference with respiration and deglutition, stiffness of the 
neck, sometimes hoarseness, and a doughy tumor in the pos- 
terior wall of the pharynx which can be detected with the 
finger before it can be seen. It should be incised in the 
median line at once. 



ACUTE ESOPHAGITIS 

Occurs practically only as the result of swallowing hot or cor- 
rosive liquids. It is marked by pain beneath the sternum, 
especially on swallowing; or in severe cases deglutition may 
become impossible. The treatment is limited to swallowing 
bits of ice or bland drinks, the use of nutrient enemata, and 
the administration of such remedies as arsenic, belladonna, 
mercury, and rhus tox. 



STENOSIS OF THE ESOPHAGUS. 

Etiology. — The obstruction may be : 

1. Spasmodic, occurring in hysterical patients, and in hydro- 
phobia, chorea, and epilepsy. 

2. Organic, due to the pressure of a tumor, sometimes an 
aneurism, on the esophagus, to a neoplasm (usually carci- 
noma) of the esophagus itself, to the presence of foreign 
bodies, or to a cicatricial narrowing of the tube following 
ulceration (corrosive poison or syphilis). 



DISEASES OF THE DIGESTIVE SYSTEM. 239 

Symptoms. — Difficuty in deglutition, regurgitation of food, 
and dilatation of the esophagus above the point of obstruction 
may be noted. 

Diagnosis. — A spasmodic stricture is usually paroxysmal, is 
associated with neurotic symptoms, and is accompanied with 
little or no nutritional failure. A bougie may be stopped at 
the seat of spasm, but in a few moments it can be passed on 
without the use of force. An organic stricture, on the other 
hand, is accompanied by a history of esophageal ulceration, 
which has been followed by the gradual appearance and per- 
sistence of the stenosis, and the obstruction to the passage 
of the bougie is permanent. The latter instrument must never 
be introduced until the possibility of an aneurism has been ex- 
cluded. 

Treatment. — The treatment of spasmodic stenosis is that of 
the causal disease. Organic stricture is, however, a serious 
and often fatal malady. If the cause is not cancerous or 
aneurismal, dilatation with graduated sounds should be at- 
tempted. 



DISEASES OF THE STOMACH AND INTESTINES. 

Disorder of the stomach is usually attended by symptoms refer- 
able to that organ, and especially in connection with the 
ingestion of food. The patient complains of actual pain or 
more often disagreeable sensations in the epigastric region, 
and there may be weight and burning after meals, flatulence, 
eructations, nausea, or vomiting. 

Disordered appetite is common, and a bad taste in the mouth 
is remarked, especially in connection with the acute, often 
gouty, gastritis popularly known as "biliousness." Thirst 
may be a symptom of gastric disease, but it is also associated 
with diabetes, and any rapid loss of fluids such as occurs by 
vomiting, purging, hemorrhage, or \>y evaporation in fever. 

Mental depression, headache, and vertigo, as well as palpita- 
tion and hiccough, are frequently the result of disordered 



240 DISEASES OF THE DIGESTIVE SYSTEM. 

digestion. The presence of constipation or diarrhea may indi- 
cate that the intestines are involved in the disease. Disorder 
of the bowel may also be made evident by such symptoms as 
colicky pain, flatulent distention of the abdomen, and various 
changes in the character of the stools. 

In some cases impaired nutrition is the only symptom of 
stomach or intestinal disease. 

Interrogation of the Patient. — Should the symptoms elicited by 
general interrogation suggest disease of the gastro-intestinal 
tract, inquire particularly in regard to: 

1. Appetite. — Is it diminished or lost, or is it excessive? 
Does it disappear after a few mouthfuls of food? Does he 
become hungry after a meal? Does he suffer with thirst? 

2. Meals. — What is their arrangement and character? Does 
he eat between meals? 

3. Abnormal Sensations. — What is their nature, and exactly 
where are they felt ? Are they produced or relieved by taking 
food? How long after eating do they come on? Are they 
influenced by the kind of food ? 

4. Belcliing. — Is there much belching, and if so, when? Is 
it after food only, or between meals? Has the gas any odor? 

5. Regurgitation. — Does the food ever come up into the 
mouth? If so, is it sour or hot? How frequently does it 
occur, and how long after meals ? 

6. Vomiting. — How often does it occur? Is it soon after a 
meal, or at other times? Does it ever occur at night? Does 
it relieve pain or not? Does he strain or retch much, or does 
it come up easily? What is the amount, color, and taste of the 
vomited matter? Does it smell bad? Was there ever any 
blood (either red blood or "coffee-grounds") in it? 

7. Boivels. — How often are they opened? What is the 
character of the stools? Is there much passing of gas? 

8. Diarrhea. — What is its frequency? What is its relation 
to meals and to special articles of food? Do the stools ever 
contain blood or slime? Does he strain during defecation? 



DISEASES OF THE DIGESTIVE SYSTEM. 241 

9. Constipation. — Is it habitual? How often are the bowels 
opened ? Is there any grooving or flattening of the stools ? Is 
there any griping pain? Does constipation alternate with 
diarrhea ? 

10. Pain in the abdomen. Is it intermittent or continuous? 
Where is it felt worse ? Is it aggravated or relieved \>y pres- 
sure ? 

Examination of the Patient. — Having completed the interroga- 
tion of the patient, the examination should begin with a 
thorougli investigation of his Jieart, lungs, and kidneys ; for in 
a large proportion of cases digestive disorder is secondary to 
diseases of those organs. This should be followed by an in- 
vestigation directed to the gastro-intestinal system itself, 
beginning with: 

External Examination. — Note the general appearance of 
the patient; emaciation and cachexia are important. Inspect the 
oral cavity; a coated tongue, bad teeth, an elongated uvula, or 
a pharyngeal catarrh may bear an important relationship to 
gastric symptoms. The contour of the stomach, its displace- 
ment, or its association with a tumor, is often discovered by 
simple inspection of the abdomen. Frequently it is advisable 
to examine the rectum through a speculum. 

Palpate the abdomen with the tips of the fingers while the 
patient lies at ease; this will disclose points of localized sensi- 
tiveness and of resistance. The position of abdominal organs 
other than the stomach is determined by the left hand push- 
ing the organ toward the palpating right hand; in this way the 
spleen or liver, if enlarged, and the kidney, if displaced, can 
be made out. Palpation of the abdomen with the patient in 
the knee-chest position is sometimes of great value. Intestinal 
symptoms frequently demand that the inquiry be extended to 
the rectum. Digital examination of the latter should be made 
with the patient in different positions, and in certain cases — for 
instance, when there is reason to suspect a malignant growth 
high up — the whole hand may be introduced while the patient 
is under the influence of a general anesthetic. 

16 



242 DISEASES OF THE DIGESTIVE SYSTEM. 

Percuss lightly to determine the position of the stomach. 
As it and the adjacent intestines are generally filled with air, 
it has been advised by some clinicians that the patient drink 
a large quantity (a quart) of water, so that the resulting dul- 
ness can be outlined. Another method, often objectionable, 
; s that of administering a small teaspoonful of tartaric acid 
in solution and immediately afterwards a similar quantity of 
sodium bicarbonate, so that the resulting gas will balloon the 
stomach. The best practical method, however, is to insert a 
tube with an attached bulb, by means of which air can be 
forced in and the stomach distended. Auscultatory percussion 
may be used; the stethoscope is placed in the angle between 
the xiphoid cartilage and the left costal margin, and the exam- 
iner after determining the note over the stomach by light per- 
cussion, begins at the middle of the abdomen and percusses 
upward toward the umbilicus until a note similar to the first 
is heard. This may be a valuable aid in mapping out the 
organ. 

Otherwise, auscultation is of little value in stomach exami- 
nations. The deglutition sounds heard at the ensiform carti- 
lage evidence the permeability of the cardia. Over the intes- 
tines auscultation is used to determine the presence of peris- 
taltic movements; absence of the normal gurgling sounds indi- 
cates paralysis of that part of the bowel, and if their 
absence is general, the complete intestinal paresis of diffuse 
peritonitis is undoubtedly present. 

Examination of the Stomach Functions. — In many cases 
interrogation of the patient, aided by the external examination, 
will afford sufficient information for a correct diagnosis. If 
any doubt remains, however, it is essential to investigate the 
secretory, absorbent, and motor functions of the stomach. 

Secretory functions. — As an aid in determining the secretory 
activity of the stomach, it is customary to administer a test 
meal (generally a test breakfast), consisting of one unbuttered 
roll or a slice of bread, and a cup of water or weak tea. One 
hour later this is removed through a tube and examined 
macroscopically and chemically. For this purpose, elaborate 



DISEASES OF THE DIGESTIVE SYSTEM. 243 

quantitative analyses may be made, but practical results are 
obtained in a few minutes by the method here outlined. 

Withdrawal of the Stomach Contents. — The patient is seated 
in a chair with a towel or apron about his neck, and he holds 
a wide-mouth bottle in his hand. The soft rubber stomach 
tube, about a yard in length, has several openings at the lower 
end and a small glass tube at the upper end. The physician 
dips this rubber tube in warm water, places the glass end in 
the bottle, tells the patient to open his mouth, and inserts the 
tube to the pharynx. Then the patient is told to swallow 
once or twice, and the tube is quickly pushed into the 
stomach. The desire to gag is overcome if the patient takes 
deep breaths. A towel wrapped around the tube will prevent 
saliva from running into the receptacle. 

The contents of the stomach may then be withdrawn by 
aspiration, a rubber bulb being attached to the tube; but as a 
rule it is enough to have the patient take a deep inspiration 
and then compress his abdominal walls in the same manner 
as during defecation. The pressure thus exerted upon the 
gastric contents expels them through the tube into the bottle. 
When removing the tube, close the glass opening with the 
ringer, lest some of the contained particles slip into the 
trachea. 

The fluid withdrawn contains a sediment of partially digested 
bread. If fermentation is occurring in the stomach there will 
be a layer of foam on the surface and an odor of butyric acid. 
If any considerable quantity of mucus is present, it can be 
partly lifted from the surface with a glass rod. 

Chemical Examination of the Stomach Contents. — A small 
quantity of the contents is allowed to pass through filter paper. 
A porcelain dish is placed under a Mohr's burette (50 c.c.)„ 
the latter being filled with a decinormal soda solution. 

Test i. Free Hydrochloric Acid. — Place 5 c.c. of the filtered 
stomach contents in the dish, together with a drop or two of 
dimethyl-amido-azo-benzol (/4 of one per cent, alcoholic solu- 
tion). If this becomes pink, free hydrochloric acid is present. 



244 DISEASES OF THE DIGESTIVE SYSTEM. 

Add the soda solution drop by drop until the hydrochloric acid 
is neutralized and the yellow color returns; the number of c.c. 
of soda solution used indicates the amount of hydrochloric 
acid present. 

Test 2. Organic Acids. — To the same 5 c.c. of contents add 
a few drops of a congo red solution (1%); if any further free 
acid is present, this turns violet. The free hydrochloric acid 
having- already been neutralized, such free acid must be 
organic; its amount is estimated by the number of c.c. of soda 
solution necessary to restore the red color. 

Test 3. Combined Acid. — Add a few drops of phenol-phtalein 
(1% alcoholic solution) and continue the addition of the soda 
solution drop by drop until the resulting pink color becomes 
no deeper and does not disappear on shaking. The result 
represents the amount of the combined acid and acid salts. 

Estimation of the Acidity. — As the tests are made with 5 
c.c. of stomach contents, it is necessary to multiply the results 
by 20 to equal the percentage of 100 c.c. This having been 
done, in normal cases the free hydrochloric acid (test 1) should 
be from 10 to 15, there should be no organic acids (test 2), 
and the combined acids (test 3) should be from 40 to 50. The 
sum of the results represents the total acidity. 

Lactic acid. — The lactic acid forming bacilli do not grow in 
the presence of free hydrochloric acid (test 1); and so if the 
latter is present no test for lactic acid is necessary. If free 
hydrochloric acid is absent, however, and the congo red reac- 
tion (test 2) is positive, it is necessary to resort to: 

Test 4. — Mix one drop of tincture of iron with enough water 
to leave a barely perceptible color, and divide the liquid be- 
tween two test-tubes. Retaining one for comparison, to the 
other add a few drops of the filtered stomach contents; a 
yellow color indicates lactic acid. For delicate testing, an 
extract made by shaking the stomach contents with ether 
should be used instead of the contents themselves. 

Blood. — Should blood, either by its fresh red color or in the 
form of brown "coffee grounds," be unrecognizable, and yet 



DISEASES OF THE DIGESTIVE SYSTEM. 245 

its presence be suspected, shake up the stomach contents,, 
allow them to settle but a few seconds, and pour off a small 
quantity from the top for microscopical examination; or else 
resort to: 

Test 5. — Mix 5 c.c. of the filtered contents with 3 c.c. of 
glacial acetic acid and add 5 c.c. of ether. Shake well, set 
aside until the ether rises to the top, and pour the latter off. 
To it add a few drops of tincture of guaiac and a small amount 
of hydrogen dioxide. A dark blue color indicates the presence 
of blood. 

Absorbent Function. — Administer 3 grains of potassium 
iodide in a gelatin capsule, being careful to wipe the outside 
clean, and then examine the saliva every minute or two for 
iodine. This is done by moistening strips of starch paper 
with the saliva, and adding a drop of fuming nitric acid; a 
slightly blue color indicates the presence of iodine. Normally 
the reaction should appear in from 8 to 15 minutes. 

Motor Function. — Wash the stomach out in the morning 
before breakfast, the patient having eaten a hearty meal the 
night before; or wash it out two or three hours after the test 
breakfast. If any notable quantity of food is found in either 
case, it shows that movement through the stomach is retarded. 

Signiiicance of the Results. — The information secured by testing 
the functional activity of the stomach, while rarely pathog- 
nomonic, is of great importance in differentiating the various 
diseases. 

1. Changes i?i the quantity of hydrochloric acid simply indi- 
cate variations in the glandular activity of the stomach. This 
may be functional, the result of neurotic conditions, or or- 
ganic. An increase of hydrochloric acid is usually functional 
(hyperchlorhydria) but it may lead to organic lesions (e. g. % 
gastric ulcer). A decrease in the quantity of hydrochloric 
acid may also be functional (neurotic), but more often it is 
due to organic disease, such as cancer or chronic gastritis. A 
coincident excess of mucus indicates the latter. Marked varia- 
tions in the quantity of hydrochloric acid indicate a nervous 
form of dyspepsia. 



246 DISEASES OF THE DIGESTIVE SYSTEM. 

2. The presence of organic acids (lactic, acetic, butyric) is 
abnormal one hour after the ingestion of the food, and sug- 
gests either carbohydrate fermentation, due to a lack of the 
digestive juices (atrophic stage of chronic gastritis; cancer), 
or long retention, as the result of motor insufficiency (dilata- 
tion of the stomach). 

3. Persistent diminution of the total acidity, especially if 
associated with absence of free hydrochloric acid, indicates 
glandular atrophy. If lactic acid is present, it favors a diag- 
nosis of gastric cancer. 

4. An excessive quantity of stomach contents (the normal 
return from a test meal is from 60 to 100 c.c. ) indicates either 
excessive secretion or pyloric obstruction The latter is often 
evidenced by exaggerated peristaltic movements visible 
through the abdominal wall. Occasionally simple muscular 
asthenia is present, in which case the test for motor activity 
will afford enlightenment. 

5. Blood may be present in the stomach contents from 
many causes. It may indicate the existence of a gastric ulcer, 
gastric cancer, acute gastritis (especially toxic gastritis), the 
passive congestion of the viscera secondary to heart disease or 
cirrhosis of the liver, or rupture of an atheromatous artery. 
For a complete list of the possible causes, see the etiology of 
Hematemesis. 

6. The absorptive power of the stomach is decreased in 
cases of atrophic gastritis, cancer, and dilatation. 

7. The motor activity is lessened in cases of dilatation, 
cancer, and the atonic form of nervous dyspepsia. 



EXAMINATION OF THE FECES. 

The average healthy adult passes one stool daily, but varia- 
tions from two or three a day to one every two or three days 
are not unusual. The color and consistence of the stools also 
vary according to the individual, and allowance for the pa- 
tient's habit must precede any deduction derived from the 



DISEASES OF THE DIGESTIVE SYSTEM. 247 

character of the feces. Generally the normal stool is solid or 
mushy and varies in color from light yellow to dark brown or 
green. 

Pathological stools may be changed in respect to: 

1. Consistence. — Liquid stools characterize diarrhea and are 
due to rapid passage of the contents of the small intestines 
through the large bowel. Early frothy stools of yellow or 
green hue may change later in the course of diarrhea to an 
offensive brown fluid, or else they may become colorless and 
resemble "rice water," as in cholera and arsenical poisoning. 
The presence in liquid stools of hard round scybalse indicates 
a diarrhea excited by fecal accumulation. 

Firm stools, often exceedingly hard and dry, characterize 
constipation; sometimes they become rounded by long deten- 
tion in the large bowel. They may be streaked with fresh 
blood from the rupture of hemorrhoidal tumors in the rectum, 
or tearing of the sphincter during their passage. 

2. Color. — Diet affects the color of the stools, a milk diet 
causing light yellow, and one of meat leading to dark brown 
stools. Some drugs, such as iron and bismuth, color the stools 
black; calomel renders them green, and rhubarb, santonin, 
and senna make them yellow. Altered blood, the result of 
hemorrhage high up in the intestine, renders the stools black, 
tarry, and offensive. If the influence of food or drugs and the 
presence of blood or pus can be excluded, changes in the color 
must be attributed to alterations in the quality or the quantity 
of the bile present. Green stools are seen early in many 
diarrheas, especially those of children. Small yellowish-white 
masses may suggest the presence of undigested casein, but if 
they are dissolved by ether, they are fatty. Fatty stools, 
sometimes appearing like tallow, occur in connection with 
amyloid disease, tuberculosis, pancreatic disease, and atrophy 
of the intestinal mucous membrane. White, clayey stools, 
which also owe their color to the fat they contain, are often 
seen in connection with obstructive jaundice or deficient bile 
formation. 



248 DISEASES OF THE DIGESTIVE SYSTEM. 

3. Odor. — The stools of breast fed infants are normally sour 
in smell. Infantile intestinal catarrhs may also occasion this 
odor; or it may become cadaverous, as a result of dysenteric, 
syphilitic, or cancerous diseases of the rectum. The absence 
of bile seems to cause an offensive odor of the stools. 

4. Abnormal Constituents. — Blood from the rectum is bright 
red and streaks the surface of the stool; it may be due to 
hemorrhoids, or to inflammation or malignant ulceration of 
the rectum or colon. Blood entering the bowel higher up 
becomes mixed with the feces; it may be brownish-red, black 
and tarry, or it may resemble coffee grounds, and its presence 
suggests intense congestion or ulceration of the stomach or 
bowels. In case there is doubt as to its presence, mix a por- 
tion of feces (rubbed up with water and filtered, if necessary) 
with a few c.c. of glacial acetic acid, and then shake with 
ether. If the ether does not settle down clear, add a few 
drops of absolute alcohol. A bronchial red color of the layer 
of ether indicates the presence of hematin acetate, i. e., of 
blood. 

Pus may be recognized in the stool in exceptional cases. 
Ulcers of the small intestine may give rise to small grayish- 
white masses composed of pus cells and mucus. The rupture 
into the bowel of an abscess is sometimes followed by the dis- 
charge of a large quantity of pure pus. 

Concretions, such as gall-stones and enteroliths, as well as 
foreign bodies and parasites, are best discovered by washing 
the feces with running water over a linen sieve. 

Microscopical examination of the feces, while of limited 
value, may occasionally afford useful information. In addition 
to particles of food (muscle and elastic fibres, fat drops, vege- 
table cells) and the epithelial cells, blood corpuscles, crystals, 
and debris from the intestine itself, it may be possible to 
recognize parasites and bacteria. For the identification of the 
latter, of which the more important are the bacilli of cholera, 
typhoid, and tuberculosis, culture methods are often necessary. 



DISEASES OF THE DIGESTIVE SYSTEM. 249 

ACUTE GASTRITIS. 

Etiology. — Acute inflammation of the stomach may be — 

1. The result of dietetic errors (food of improper character, 
excessive in amount, or too hastily swallowed; alcohol; iced 
drinks, etc.). 

2. An accompaniment of acute infectious diseases. 
Pathology. — The mucous membrane becomes red, swollen, 

covered with mucus, and sometimes eroded. 

Symptoms. — Epigastric distress, nausea, and vomiting of 
food, mucus, and bile usher in the attack. There may be some 
pyrexia, the tongue is coated, and headache and other febrile 
symptoms are present. Should the stomach not succeed in 
emptying itself by vomiting, the intestines become involved. 
In consequence a diarrhea is set up, and it is accompanied 
with more or less abdominal pain and tenderness. 

Diagnosis. — Typhoid fever and other oncoming infections 
may be simulated by febrile cases of acute gastritis, but the 
latter always terminates within a week. In doubtful cases, 
the existence of herpes labialis favors a diagnosis of gastritis; 
the occurrence of the diazo-reaction, typhoid. 

Biliaiy colic is accompanied by greater pain, which is located 
about the gall-bladder or ducts, and jaundice is frequently pres- 
ent. 

Prognosis. — Recovery usually occurs within five days. 

Treatment. — Often the attack can be subdued immediately 
by placing the patient in a warm bath and adding as much hot 
water as can be borne; continue the bath for half an hour or 
more. Vomiting rids the stomach of offending food, and on 
that account should be encouraged; if it is necessary to aid 
nature, let the patient drink a pint of lukewarm water and 
tickle the fauces. The stomach having been emptied, permit 
no food for a day, and then begin feeding cautiously with milk 
and soups. During the acute stage small quantites of water 
or bits of ice may be swallowed in order to quench the thirst. 



250 DISEASES OF THE DIGESTIVE SYSTEM. 

Of remedies, apomorphia or ipecac may be required to con- 
trol excessive vomiting; unusual prostration will suggest 
arsenic; and mix vomica will be indicated by a history of 
dietetic errors or alcoholism. A heavily coated tongue with 
great nausea and pain suggests the administration of antimon. 
crud., bilious vomiting with intense distress in the epigastrium 
is relieved by iris, Pulsatilla is used in attacks brought on by 
indulgence in fats or acids, and bryonia in those cases which 
result from over-indulgence in cold drinks. Cuprum ars. is 
almost specific in cases in which intestinal involvement is 
indicated by the onset of colic and diarrhea. 

Acute Toxic Gastritis, the intense inflammation of the stomach 
which follows the ingestion of irritant poisons (arsenic, acids, 
corrosive sublimate, etc.), is attended with severe symptoms 
of sudden onset, including pain, vomiting and collapse, The 
diagnosis is often made after questioning the patient or by de- 
tecting traces of the poison about the mouth or in the vomitus. 
Treatment must include the appropriate antidote, followed by 
rest and probably rectal feeding until the eroded stomach 
walls can heal. 

Phlegmonous Gastritis, a rare suppurative inflammation of the 
stomach, occurs by metastasis in pyemic and other septic 
states, and sometimes it is apparently idiopathic. It is at- 
tended with severe pain, high fever, and complete anorexia, 
and death ensues within a week or two. Diagnosis during life 
is impossible. 

CHRONIC CATARRHAL GASTRITIS. 

Etiology. — Chronic catarrhal inflammation of the stomach 
may be induced by — 

1. Dietetic errors. 

2. Repeated attacks of acute gastritis. 

3. It may be a symptom of heart, lung, liver, or kidney 
disease. 

Pathology. — The mucous membrane is of a yellow or slate 



DISEASES OF THE DIGESTIVE SYSTEM. 251 

color, sometimes presenting ecchymotic spots, and covered 
with mucus. Microscopically it may be seen that the disease 
has begun as a glandular inflammation, and this has been 
followed by interstitial changes. Atrophy of the mucous 
membrane, with complete glandular destruction, may finally 
ensue. 

Symptoms. — The disease is of gradual development, and at 
first the symptoms are obscure. There may be a disagreeable 
taste in the mouth, bad breath, a coated tongue, deranged 
appetite, and a sense of epigastric fulness which at times leads 
to palpitation and dyspnea. Belching, vertigo, and headache 
are common, but pain is generally absent. Vomiting is not 
usual; when it occurs, it is apt to be in the morning. The 
bowels are constipated as a rule, and the urine is scanty and 
deposits urates and phosphates. 

The general symptoms include languor, irritability, mental 
inactivity, and a desire to yawn. As a rule, the patient appears 
well nourished, but late in the course of the disease consider- 
able emaciation may take place. 

Gastric Contents.— Examination of the stomach contents 
one hour after a test meal shows lessened acidity, little or no 
free hydrochloric acid, and often much mucus. 

Diagnosis. — The long continuance of the symptoms described, 
and the low acidity of the stomach contents, associated often 
with an excessive quantity of mucus, render the diagnosis 
clear. 

Ulcer and cancer are generally distinguished by severe pain, 
hematemesis, and emaciation; in the case of ulcer there is a 
circumscribed tender spot in the epigastrium, and in cancer 
the tumor may be detectable. 

A gastric neurosis may present symptoms suggestive of 
chronic catarrhal gastritis, but the coexisting nervous disturb- 
ances and the sudden changes in the subjective sensations and 
in the chemical condition of the gastric contents will aid in its 
recognition. 

Prognosis. — The disease is of long duration, and becomes 



252 DISEASES OF THE DIGESTIVE SYSTEM. 

more serious in proportion to the decrease of gastric secretion. 
If the condition is not secondary to some incurable disease of 
another organ, recovery or at least improvement is generally 
possible; but relapses are common. Chronic gastritis tends 
to complete destruction of the secreting structures (achy Ha 
gastricd) and dilatation of the stomach, and these changes 
represent an incurable condition. 

Treatment. — When a patient submits himself to treatment, 
for the first week or two his meals must be regular, carefully 
masticated, and very light (milk, koumyss, oatmeal, rice and 
chicken soups, soft boiled eggs, mashed potatoes, scraped 
meat, and toasted bread). Then the amount of food must be 
increased gradually, and he must continue to abstain from in" 
digestible food, alcohol, and tobacco. Rest after meals, regu- 
lar hours of sleep and rest, moderate open air exercise, and a 
morning sponge bath should be enjoined. A tumblerful of hot 
water half an hour before each meal serves to clear the stom- 
ach of mucus; but in severe cases daily lavage followed by the 
administration of a pint of peptonized milk affords a preferable 
method of accomplishing this result. The drinking of a few 
spoonfuls of hydrogen dioxid, somewhat diluted, followed in a 
few moments by the ingestion of a pint of hot water, is often 
equally effective. It in turn should be followed by the admin- 
istration of peptonized milk. 

Of medicines, nux vomica is particularly useful in atonic, 
constipated patients by whom purgatives have been abused. 
Hydrastis is indicated by the presence in the stomach of 
excessive quantities of mucus, with vomiting, constipation, 
and often a ''sinking" sensation in the epigastrium. Pulsa- 
tilla may be given in similar cases in which flatulence and 
eructations have been brought on by indulgence in rich food. 
Obstinate cases with great flatulence, vomiting of mucus, and 
epigastric distress are relieved by argentum nit. Arsenic is 
indicated by extreme gastric irritability, with burning pain, 
thirst, restlessness, and anxiety; while bryonia is suitable for 
cases presenting great dryness of the digestive tract, the un- 



DISEASES OF THE DIGESTIVE SYSTEM. 253 

digested food causing a sense of weight in the stomach, to- 
gether with constipation and liver disturbance. 

Lycopodium (flatulent, lithemic patients), sepia (neurotic 
women of gouty habit), cincliona (patients debilitated by 
acute diseases), and sulphur (chronic gastritis associated with 
liver disease and hemorrhoids) are also remedies of value. 

Carbolic acid in doses of 2-5 drops, well diluted, of a one 
per cent, watery solution, administered after cleansing the 
stomach, is a remedy of great value, particularly in gastric 
catarrhs of alcoholic origin. Great flatulence may justify the 
administration of bismuth subgallate or sodium sulphocarbolate 
in 5-10 grain doses after meals. 



ULCER OF THE STOMACH. 

Etiology. — A gastric ulcer may be due to: 

1. Malnutrition of the mucous membrane of the stomach 
(anemia, chlorosis, heat, or kidney disease, etc.). 

2. Local thrombosis and embolism, the resulting blood stasis 
permitting digestion of the membrane by the gastric juice. 

3. Hyperchlorhydria. 

4. Mechanical injury (by pressure, as in shoe making). 

5. Predisposition (young women). 

Pathology. — The digestion of a portion of the mucous mem- 
brane by the gastric juice leaves a round, funnel-shaped ulcer 
of varying depth. Generally it is situated on the posterior 
wall of the greater curvature of the stomach. Rarely the 
ulcers are multiple. 

Course. — 1. The ulcer may cicatrize. This termination, usu- 
ally favorable, may nevertheless lead to contraction and steno- 
sis at the pyloric orifice; or the cicatricial tissue may later be- 
come the seat of malignant disease. 

2. The ulcer may persist for years without healing. 

3. The ulcer may penetrate the stomach wall, the gastric 
contents entering the peritoneal cavity and causing a rapidly 
fatal septic peritonitis. 



254 DISEASES OF THE DIGESTIVE SYSTEM. 

4. Adhesions may form between the stomach and the ad- 
jacent viscera (liver, pancreas, omentum) preventing or at 
least localizing the peritonitis. 

5. Fistulous tracts into these adjacent viscera, or into the 
pleura or pericardium, may be formed. 

6. Erosion of a blood vessel may occur; the gravity of the 
ensuing hemorrhage varies according to the size of the vessel 
thus opened. 

Symptoms. — Many cases of gastric ulcer present no special 
symptoms; the lesion may be discovered only at autopsy fol- 
lowing death from other causes. In typical cases, however, 
the disease is characterized by: 

1. Pain, especially, but not necessarily, after taking food, 
and often relieved by vomiting. 

2. Tenderness on pressure over the ulcer. This is strictly 
localized to a small spot, which is often an inch or two above 
the umbilicus. 

3. Vomiting, shortly after eating, the vomitus usually con- 
taining an excess of hydrochloric acid. 

4. Hemorrhage, which is often quite profuse and leads to 
vomiting of bright red blood or the passage of tarry stools. 

5. Anemia, usually of chlorotic type, accompanied by 
progressive emaciation. 

6. General dyspeptic symptoms. These are present in vary- 
ing degree, and in some cases constitute the only signs of the 
disease. 

7. Gastric Contents. — The stomach tube must not be used; 
but examination of the vomitus usually discloses great hyper- 
acidity of the gastric juice. 

Diagnosis. — In gastralgia the pain is irregular in its occur- 
rence, without aggravation by food; localized tenderness, 
vomiting, hematemesis, and dyspeptic symptoms are absent, 
and the neurotic character of the patient is usually evident. 

Chronic gastritis lacks the severe pain, frequent vomiting, 
hematemesis, and anemia, which usually characterize cases of 



DISEASES OF THE DIGESTIVE SYSTEM. 255 

gastric ulcer, while the amount of hydrochloric acid in the 
stomach contents is decreased. 

In hyperchlorhydria the pain is apt to appear two or three 
hours after the ingestion of food, and it is relieved by the 
administration of more food or of an alkali, such as sodium 
bicarbonate; waterbrash is frequently present and hemate- 
mesis does not occur. 

Cancer occurs later in life; the pain is less intense but more 
continuous, the amount of blood vomited is comparatively 
small, and often the vomitus betrays the absence of hydro- 
chloric and the presence of lactic acid. The appearance of 
cachexia and the discovery of a palpable tumor afford conclu- 
sive evidence as to the nature of the lesion. 

Prognosis. — This must be guarded, since fatal hemorrhage or 
perforation is possible at any time, and relapse even after 
apparent recovery is not unusual. Treatment is effective in 
recent cases, a large proportion of which recover. 

Treatment. — 1. Rest. Put the patient to bed. 

2. Diet. For a period of a week or ten days, severe cases 
require rectal feeding (peptonized milk, beef juice, or pep- 
tones, four ounces every 4-6 hours). Milder cases may be 
given peptonized milk by the mouth (two ounces every two 
hours), and beef peptone and egg albumen may be substituted 
gradually or in part. As the symptoms subside, thin gruels, 
raw eggs, well-cooked rice, and custards are permitted, but 
the return to solid food must be very gradual. 

3. Medicines. Atropine, 3x, controls as by magic the severe 
pain of a gastric ulcer associated with hyperchlorhydria 
(Goodno). Argent, nit., in freshly-made watery solution, is an 
invaluable remedy when there is epigastric pain and belching 
of great quantities of gas. Arsenic is useful when its charac- 
teristic thirst, burning pain, vomiting, and prostration are 
present. Kali Inch, is suggested by catarrhal symptoms and 
vomiting of thick mucus, while Hydrastis is suited to catarrhal 
cases with sensations of weakness and aching and cutting 
pains in the epigastrium, together with loss of appetite. The 



256 DISEASES OF THE DIGESTIVE SYSTEM. 

distinct etiologic relationship of hyperchlorhydria to ulcer of 
the stomach renders the treatment advised for the former con- 
dition equally applicable to many cases of gastric ulcer. 

Hemorrhage may be met by the use of ice externally and in- 
ternally, small bits being swallowed by the patient, and the 
administration of ipecac, hamamelis, or hydrastinine hydro- 
chlorate. Severe hemorrhage or symptoms of perforation may 
require morphia, gr. %, hypodermatically; and at times sur- 
gical intervention is advisable. 

CANCER OF THE STOMACH. 

Etiology. — Heredity, mature life, gastric catarrh, and ulcer 
are among the conditions which predispose to cancer. 

Pathology. — Excepting the female generative organs, the 
stomach is the organ most frequently attacked by primary 
cancer; rarely it is secondary. The growth originates in the 
mucous coat; any variety may occur, but the more frequent 
are the cylinder-celled epithelioma, medullary, scirrhus, and 
colloid. It may appear as a projecting tumor, a diffuse in- 
flammation, or an annular constricting band, situated either at 
the pylorus (60%), the cardia (10%), or over the greater or 
lesser curvature. The location of the growth affects the shape 
of the stomach, dilatation following obstruction at the pylorus, 
or contraction resulting from stenosis at the cardia. The in- 
creased weight of the stomach and its adhesions to adjacent 
organs may serve to displace it. 

Symptoms. — These are often obscure, but as a rule they 
develop somewhat in the following order: 

1. Dyspeptic symptoms, perhaps with sudden loss of appe- 
tite. 

2. Failure of general health, with increasing weakness and 
emaciation; finally cachexia. 

3. Epigastric pain, constant and increasing in severity. 

4. Vomiting, often of retained food which has become 
offensive, and which may be admixed with blood in small 
quantities. 



DISEASES OF THE DIGESTIVE SYSTEM. 2d i 

The position of the growth may occasion some variation in 
the symptoms, e. g. } a cancer at the car'dia causes pain and 
difficult}- in swallowing. 

Stomach contents. Chemical examination of the vomitus 
reveals absence or a minimum amount of hydrochloric acid, 
and lactic acid is often present. Washing out the stomach 
in the morning will reveal the presence of undigested food 
from the meals of the previous day, indicating pyloric stenosis. 
Microscopical examination may reveal a small amount of 
blood or particles of the malignant growth. 

Physical Examination. — The tumor is palpable when situated at 
the pylorus or on the anterior wall or greater curvature. Me- 
tastatic involvement of glands, nodular infiltration of the liver 
or of the thoracic viscera, with indications of pleurisy, may be 
noted. A cancer situated at the cardia often leads to stenosis 
of the esophagus, with absence of the deglutition sounds at 
that point. 

Clinical Course.— 1. Generally, death from exhaustion ensues 
within two years. 

2. The disease, particularly in the aged, may run a latent 
course, death finally resulting from some intercurrent dis- 
order. 

3. The gastric condition may be masked, the symptoms 
suggesting the possibility of pernicious anemia or nephritis. 

4. Secondary growths of the liver or peritoneum may ob- 
scure the primary lesion. 

Diagnosis. — The diagnosis of cancer of the stomach is fraught 
with difficulty; almost ever}' symptom may be present, and 
3 T et be due to other causes, and in other cases characteristic 
signs of the disease may be utterly lacking, only autopsy reveal- 
ing the presence of the neoplasm. The symptoms and signs 
distinguishing cancer from other gastric diseases have been 
considered in connection with ulcer of the stomach. 

Abdominal tumors not originating in the stomach can be 
distinguished by careful physical examination as to their 
attachments. 
. 17 



258 DISEASES OF THE DIGESTIVE SYSTEM. 

Benign tumors of the stomach are rare, and their presence 
give rise to no malignant symptoms. 

Dilatation of the stomach due to benign stenosis of the 
pylorus affords a history of long illness interrupted by periods 
of almost complete freedom from symptoms. 

Prognosis. — Hopeless; death almost inevitably occurs within 
three years. 

Treatment. — Nourish the patient with easily assimilable food. 
Palliate the pain with morphia or svapnia. Control vomiting 
with ice, champagne, and appropriate medicines. Lavage 
may be used to clear the stomach of irritating undigested 
food. When stenosis becomes extreme it is necessary to 
resort to rectal feeding. 

Surgical interference, though hazardous, may be considered. 

DILATATION OF THE STOMACH. 

(Gastrectasis.) 

Etiology. — The capacity of the stomach may become increased 
as the result of: 

1. Pyloric obstruction (pyloric tumors or cicatrices, pressure 
on the pylorus by tumors of adjacent organs). 

2. Muscular atony, due to overloading the stomach with 
food and drink, to gastric catarrh, or to diseases producing 
general atony (diseases of heart, lungs, kidneys, and blood). 

Pathology. — The stomach, normally capable of containing 
about three pints, becomes dilated to two or three times that 
capacity, with thinning of the muscles and the changes in the 
mucous membrane characteristic of chronic gastric catarrh. 

Symptoms. — The patient presents symptoms of gastric ca- 
tarrh, sometimes combined with those of the causative con- 
dition (<?. g. f tumor). In addition he vomits at intervals large 
quantities of undigested and fermenting food, which have evi- 
dently been accumulated within the stomach. If the vomitus is 
allowed to stand, a sediment of undigested food is thrown down, 
and microscopic examination reveals the presence in it of yeast 



DISEASES OF THE DIGESTIVE SYSTEM. 259 

fungi; sarcinae, and bacteria. Hydrochloric acid is generally 
replaced by lactic, butyric, and other organic acids, and the 
motor power of the stomach is lessened. 

In advanced cases general nutrition fails, the bowels become 
constipated and the urine scanty, anemia and emaciation are 
progressive, and death finally occurs from exhaustion or toxic 
absorption. Cessation of the vomiting, indicating muscular 
failure of the stomach, is often a danger signal. 

Physical Signs. — Inspection may reveal the outline of the 
bulging organ, palpation confirming the discovery. Percussion 
of the artificially distended stomach, the patient standing up- 
right, will show its excursion below the umbilicus. 

Prognosis. — This depends upon the cause. If the condition 
is due to cicatricial contraction or tumor of the pylorus, it is 
incurable, although persistent palliation is still possible; if it 
is the result of simple muscular atony, the prospect is fairly 
favorable. 

Treatment. — The patient should be restricted to a dry diet, 
consisting of grated meats, cereals, dry bread thoroughly mas- 
ticated, and prepared foods in powder form, such as somatose. 
If liquids are permitted at all, very small quantities should be 
taken at frequent intervals. Fats must be forbidden, and 
starch and sugar should be taken most sparingly. 

Cleanse the stomach by daily lavage with a mildly alkaline 
solution, followed by the ingestion of a little peptonized milk. 
Avoid constipation ; use enemata or laxatives if necessary. 

Medicines may be given in accordance with any sympto- 
matic indications present; their effects are necessarily limited 
to a control of the associated gastric catarrh, and the more 
important drugs are those recommended for that disease. 

HEMATEMESIS. 

Etiology.— Hemorrhage into the stomach, from which hema- 
temesis usually results, may be due to: 

1. Traumatism (mechanical injuries, such as blows or 
wounds; chemical injuries by acids or alkalies, etc.). 



260 DISEASES OF THE DIGESTIVE SYSTEM. 

2. Gastric diseases (ulcer; cancer; disease of the gastric 
blood vessels, including atheroma and varicose veins; and 
gastric congestion, in connection with acute gastritis, cirrhosis 
of the liver, chronic heart and lung diseases, etc.). 

3. Blood disorders (acute infectious diseases, such as yellow 
fever, smallpox, malaria, etc. ; toxemias, such as that induced 
by phosphorus-poisoning; and hemorrhagic diseases, such as 
scurvy, purpura, and hemophilia). 

4. Nervous diseases (hysteria, epilepsy, paresis) rarely. 

5. Melcena neonatorum, a profuse and fatal hemorrhage in 
the newborn. 

6. Rupture of an aneurism of the abdominal aorta into the 
stomach. 

Diagnosis. — It is essential to recognize the cause of hemor- 
rhage into the stomach, and, moreover, it is necessary to dis- 
tinguish the latter from blood swallowed during an attack of 
epistaxis or hemoptysis and later vomited or passed with the 
stool. 

Prognosis.— The hemorrhage is seldom immediately fatal; in 
other respects the prognosis depends upon the cause. 

Treatment.— Rest, abstention from food, and the use of ice 
locally are advisable. Administer such remedies as ipecac, 
hamamelis, hydrastinine hydrochlorate, turpentine, or various 
other medicines selected according to the cause and the asso- 
ciated conditions. Intravenous saline infusions may become 
necessary in extreme cases. 

GASTRIC NEUROSES. 

Etiology. — Functional disorders of the stomach, due to ner- 
vous influences, are the result of 

1. A neurotic temperament, hereditary or acquired. 

2. Neurasthenia, due to overwork, injudicious dieting, etc. 
Clinical Varieties. — Disordered innervation of the stomach 

may manifest itself in — 

1. Neuroses of sensation (nervous dyspepsia, gastralgia, 
etc.). 



DISEASES OF THE DIGESTIVE SYSTEM. 261 

2. Neuroses of secretion (hyperchlorhydria, occasionally 
hypochlorhydria or sub-acidity). 

3. Neuroses of motility (increased or diminished peristalsis) . 

These three varieties of gastric disorder resulting from dis- 
turbed innervation are not always separated one from another 
by sharp lines of demarcation, and in consequence they are 
usually classified together under the general term of ''nervous 
dyspepsia." In certain cases, however, notably that of hyper- 
chlorhydria, the neurosis presents a distinct clinical type. 

NERVOUS DYSPEPSIA. 

(Gastric Neurasthenia.) 

Symptoms. — In this form of dyspepsia the stomach is able to 
accomplish digestion within the normal seven hour limit, but 
the process is attended with annoying symptoms. The latter 
may be gastro-enteric (fulness after eating, belching of taste- 
less gas, nausea but rarely vomiting, rumbling in the bowels, 
and constipation), but they are usually associated with many 
neurotic symptoms, such as palpitation, numbness of the ex- 
tremities, and anxiety. In certain cases these symptoms are 
associated with muscular atony of the stomach and consequent 
stasis of the gastric contents {atonic dyspepsia). 

Diagnosis. — The recognition of nervous dyspepsia depends 
upon the exclusion of all organic causes, gastric or otherwise, 
for the symptoms. The neurotic association, together with 
the liability of the symptoms to appear and disappear sud- 
denly, is an aid to diagnosis. 

Prognosis. — For hfe, good; for recovery, doubtful. 

Treatment. — That of neurasthenia or hysteria: Rest, proper 
exercise, a full nutritious diet, and such remedies as argent, 
nitr., cinchona, iguatia, lycopodium, mix vomica, Pulsatilla, 
etc. 



262 DISEASES OF THE DIGESTIVE SYSTEM. 



HYPERCHLORHYDRIA. 

Etiology. — Hyperacidity of the gastric juice may be paroxys- 
mal, or it may be continuous {Reichrnanri s disease}. It 
occurs particularly in neurasthenic and gouty adults as a result 
of emotional causes, such as overwork and worry. 

Symptoms. — In the paroxysmal variety the patient suffers 
distress and pain in the stomach two or three hours after eat- 
ing, with thirst, pyrosis, eructations, and even vomiting. 
Relief can always be secured by taking food, alkalies, or large 
quantities of water. 

If uncontrolled, these symptoms tend to pass into the con 
tinuous form, in which the distressing sensations persist with- 
out intermission and are even more severe. The irritation 
leads to increased muscular activity of the stomach, the food 
being hurried on without opportunity for digestion or absorp- 
tion, and ultimately in spite of the large quantity of food 
taken, anemia and emaciation ensue. 

Course. — Hyperchlorhydria may lead to dilatation of the 
stomach, either through the irritating gastric juice causing 
spasm of the pylorus, or through atony of the weary muscular 
coat permitting accumulation within the organ. Increasing 
dilatation may ultimately lead to glandular atrophy. Ulcer of 
the stomach is an exceedingly common complication or 
sequence of long-continued hyperacidity. 

Diagnosis is possible only after an examination of the gastric 
contents. One hour after the test breakfast the contents 
show an excess of hydrochloric acid, often amounting to two 
or three times the normal amount. 

Prognosis. — The prognosis under proper treatment is favor- 
able, except in those protracted cases in which the condition 
has become continuous; the latter are rarely cured. 

Treatment. — The distress attending the attack can be relieved 
by the administration of nitrogenous food (meat and milk) or 
by neutralizing the acid with an alkali (sodium bicarbonate or 
Carlsbad salts, gr. x, every 10 minutes until relief is obtained). 



DISEASES OF THE DIGESTIVE SYSTEM. 263 

In order to radically cure the disease, however, it is neces- 
sary to regulate the habits of the patient, prohibiting over- 
work and securing for him necessary rest and out-door exercise. 
The diet must consist largely of meat, carbo-hydrates being 
reduced in quantity to a minimum; and all substances tending 
to excite the activity of the stomach glands, such as spices, 
fruits, and acids, must be prohibited. 

Of remedies, atropine 3x given just before each meal usually 
ensures almost immediate relief. Anacardium is often indi- 
cated by the constant hunger, with relief from eating, but 
aggravation in two or three hours. Robinia, cuprum ars., mix 
vomica, and iris are also extremely useful in appropriate cases. 

GASTRALGIA 

(Gastrodynia; Cardialgia; Neuralgia of the Stomach) 

Is a term properly applicable only to paroxysmal stomach 
pain unassociated with any discoverable organic lesion. It 
occurs particularly in neurotic and anemic women. For the 
exclusion of gastric ulcer and cancer, angina pectoris, the 
gastric iris of locomotor ataxia, gall-stone and intestinal colics, 
etc., careful and painstaking examination is often necessary. 
The treatment of the attack should include the application of 
external heat, the drinking of large quantities of hot water, 
and the administration of such medicines as arsenic, bella- 
donna, copper arsenite, iris, and nux vomica. 

SPLANCHNOPTOSIS. 

(Glenard's Disease.) 

Varieties. — Splanchnoptosis (visceroptosis) is a general term 
for the downward displacement of certain of the abdominal 
viscera, especially the stomach {gastroptosis), the intestines 
(enteroptosis), the kidney {nephroptosis), the spleen (splenop- 
tosis), and the liver (hepatoptosis). 

Etiology. — The displacement is the result of: 

1. Relaxation of the abdominal walls; and 



264 DISEASES OF THE DIGESTIVE SYSTEM. 

2. Loosening or overstretching of the supporting ligaments. 

The condition is usually found in young women. It has 
been attributed to undue exertion, to injuries, and to relaxa- 
tion of the abdominal walls following repeated pregnancies. 
The gastro-intestinal prolapse leads to a certain degree of 
stenosis, whereby the passage of food is interfered with and 
nutrition suffers in consequence. 

Symptoms. — The patient suffers with a general asthenia; she 
readily becomes tired, and is comfortable only when lying 
down. vShe complains of a sense of weight and a sickening 
dragging in the abdomen. Gastric symptoms are prominent — 
anorexia, distress, burning, or pain in the epigastric region, 
nausea, vomiting, diarrhea, or constipation. The symptoms 
are more or less relieved by pressure, either by the hands or a 
belt, upon the lower abdomen. 

Diagnosis.— In the presence of these symptoms, careful phy- 
sical examination of the abdomen, made while the patient 
stands erect and again when she lies down, becomes neces- 
sary. 

Among the objective signs the following are more or less 
characteristic: 

1. A splashing sound (chapotement epigastrique) in the 
stomach from two to six hours after meals. 

2. Pulsation of the abdominal aorta (battement aortique). 

3. A cord-like body lying transversely at or below the level 
of the umbilicus, supposed to be the transverse colon (pan- 
creas?). 

4. Displaced or movable abdominal organs, especially a 
floating kidney. 

Treatment. — The patient should wear an abdominal bandage 
reaching to the navel and exerting pressure upward, or, better, 
a special truss may be constructed for the purpose. The 
bowels should be kept open by means of aperients (Hunyadi, 
Rubinat, or Carlsbad water) if necessary. The tonicity of the 
abdominal walls may be improved by massage, electricity, 
hydrotherapy, and sometimes gymnastic exercises. Medicines 



DISEASES OF THE DIGESTIVE SYSTEM. 265 

should be prescribed for the dyspeptic and other symptoms as 
they present themselves. 



ACUTE ENTERITIS. 

Etiology. — Acute intestinal catarrh is usually the result of the 
action of some irritant; the disease may be primary, due to — 

1. Dietetic errors. Unripe fruit, the ingestion of food in 
too large quantities, and food decomposed as the result of 
bacterial activity. 

2. Toxic causes, e. g. y metallic poisons and drastic cathartics. 
The intestinal inflammation may be secondary to — 

1. Gastric disorders which permit irritating substances to 
pass into the intestine. 

2. Organic intestinal disorders, such as ulcer, cancer, hernia, 
and peritonitis. 

3. Congestion of the intestinal blood vessels, the result of 
portal obstruction, occurring in chronic heart and lung dis- 
eases. 

4. Acute infectious diseases, such as typhoid. 

5. Chronic cachexias (nephritis, tuberculosis, cancer, ane- 
mia). 

6. Foreign bodies, such as enteroliths, gall-stones, and 
parasites. 

Pathology. — The mucous membrane becomes hyperemic and 
swollen, and its surface is covered with mucus, desquamated 
epithelium, or even pus. The process may be localized or 
diffuse, and may be accompanied by ulcerative changes in the 
glands and erosion of the mucous membrane. 

Symptoms.— 1. Diarrhea, due to increased peristalsis and 
augmented secretion, is the principal symptom of enteritis. 
It may, however, be absent if the inflammation remains con- 
fined to the upper bowel, and the colon is not involved. The 
early bowel movements dispose of the solid masses, and as a 
result the later stools become thin and finally watery. 



266 DISEASES OF THE DIGESTIVE SYSTEM. 

2. Pain. Defecation may be preceded by colicky pain in 
the abdomen and followed by tenesmus. 

3. Among the associated symptoms may be nausea, loss of 
appetite, great thirst, abdominal tenderness, and concentrated, 
sometimes albuminous, urine. 

Diagnosis. — Generally the symptoms suffice for diagnosis; but 
as it is essential to know whether the enteritis is primary or 
secondary, careful examination for the probable causes of the 
latter is necessary. 

Exact localization of the intestinal lesion is not always pos- 
sible. Duodenal catarrh may be indicated by tenderness in 
the right hypochondrium following an attack of gastritis; the 
stools usually contain an excess of mucus, and occasionally 
jaundice is present. Catarrh of the small intestine is accom- 
panied by an excess of indican in the urine; or it may be 
indicated by Rosenbach's reaction. The latter is obtained by 
boiling urine in a test-tube while adding nitric acid drop by 
drop; a burgundy-red color which persists on further boiling 
affords positive evidence of disturbed enteric metabolism. 
Catarrh of the large intestine is accompanied by tenesmus 
and severe colicky pains in the left iliac fossa, together with 
itching and burning at the anus, the passage of mucus and 
blood, and great pain on digital examination. 

Prognosis. — Primary cases are serious only at the extremes of 
life; the prognoses of secondary cases vary according to their 
cause. 

Treatment. — Rest in bed, with enforced use of the bed pan, 
and a light diet, are essential details in the treatment of every 
case. Acute catarrh of the small intestine with little asso- 
ciated pain is usually controlled by bryonia, croton tig., cin- 
chona, colchicum, or podophyllum; great pain indicates the 
need of colocyntJi, cuprum ars., or nux vomica; and involve- 
ment of the colon suggests the administration of aloes or mer- 
curius dtclcis. Attacks resulting from improper diet, with 
various associated gastric symptoms, may require the use of 
antimon. crud., ipec, or nux vomica. Arsenic may prove use- 
ful in severe cases with great thirst, restlessness, etc. 



DISEASES OF THE DIGESTIVE SYSTEM. 26' 



CHRONIC ENTERITIS. 

Etiology. — Chronic catarrhal inflammation of the intestine is 
usually secondary to repeated acute attacks or the persistence 
of the causes therefor. 

Pathology. — The process consists of a chronic catarrhal in- 
flammation of the intestinal mucous membrane with ensuing 
hypertrophies, atrophies, and ulcerations. 

Symptoms. — 1. Diarrhea. This is not invariable, constipa- 
tion, or alternating constipation and diarrhea, being present in 
many cases. 

2. Mucus in the stools, in sago-like flakes or jelly-like masses. 

3. Blood in the' stools, when ulceration occurs. 

4. Pus in the stools. This appears when inflammation of 
the rectum (proctitis) has resulted in abscess-formation. A 
rectal fistula ma} T ensue. 

5. Nutritional disturbances. Emaciation and weakness are 
prone to occur in connection with advanced changes in the 
mucous membrane. Should an atrophic process involve both 
the stomach and bowels, a pernicious form of anemia develops. 

Diagnosis. — The passage of large amounts of mucus with the 
stools determines the condition, and its localization may be 
judged according to the signs referred to in connection with 
the diagnosis of acute enteritis. Recognition of the primary 
cause is essential. 

Prognosis. — Under any circumstances the prognosis as to 
recovery must be guarded; but it varies somewhat according 
to the cause and its removability. 

Treatment. — 1. Discover and treat the cause (heart and 
kidney diseases, etc.) 

2. Diet. Food containing a minimum of waste, i. e., milk 
and later nitrogenous substances should be given. For gouty 
and nephritic patients the latter are contra-indicated, how- 
ever, and in such cases recourse must be had to stale bread 
and well-cooked cereals. 



268 DISEASES OF THE DIGESTIVE SYSTEM. 

3. Daily irrigation of the colon with pure water, or a saline 
solution (2-3 pints), is advisable in obstinate cases involving 
that portion of the bowel. 

4. Medicines must be carefully selected after consideration 
of the cause as well as the obtrusive symptoms. Among those 
most frequently indicated are aloes, argent, nit., arsenic, cin- 
chona, mercur. cor., and sulphur. Intestinal antiseptics, e. g., 
bismuth subgallate, beta-naphtol bismuth, and sodium sulpho- 
carbolate, in doses of from five to ten grains three times a day, 
may be used in some cases. 

CHOLERA MORBUS. 

(Cholera Nostras, Sporadic Cholera) 

Cholera morbus is a severe form of acute gastro-enteritis oc- 
curring particularly in hot weather and in young adults. It is 
due to dietetic errors followed by decomposition of the gastro- 
intestinal contents and toxic absorption. The attack is charac- 
terized by the sudden onset of violent vomiting, purging, and 
pain; and severe cases closely resemble Asiatic cholera. The 
treatment should be that directed for the latter disease. 



THE DIARRHEAS OF CHILDREN. 

Etiology. — 1. Dietetic errors. The disorder is apt to occur 
in artificially-fed children because of improper or contami- 
nated food. 

2. Hot weather. This tends to aid bacterial development 
in the food, and to weaken the resistance of the child. 

3. Dentition and faulty hygiene act as predisposing causes. 

Pathology. — The condition varies from a simple non-inflam- 
matory catarrh of the small intestine {intestinal indigestion) 
to an inflammation which especially affects the lymph follicles 
of the ileum and colon (entero-co litis) or an intense gastro- 
enteritis of bacterial origin (cholera infantum). 

Symptoms. — These varieties are recognizable clinically, viz., 



DISEASES OF THE DIGESTIVE SYSTEM. 269 

1. Intestinal indigestion, characterized by slight fever, rest- 
lessness, and some purging. The stools are sour and offensive; 
at first they contain coagulated milk or other undigested food, 
but later they become greenish and watery, and often contain 
a little mucus or blood. The disorder may be acute or 
chronic; if the latter, it may lead to death from exhaustion. 

2. Enterocolitis \ the variety in which the inflammation 
especially affects the lymph follicles of the ileum and colon, is 
gradual in onset and at first suggests intestinal indigestion; 
speedily, however, it becomes severe, and is accompanied 
by high fever (104°), a distended and painful abdomen, and 
irritating stools containing large quantities of mucus. The 
child emaciates rapidly, and if the disease remains unchecked 
death occurs in a few weeks. 

3. Cholera infantum, an intense gastro-enteritis due to bac- 
terial contamination of the food, is characterized by the 
sudden onset of severe vomiting and purging, with high fever 
(105°-106°), rapid exhaustion, and often death within a few 
hours. 

Diagnosis. — In intestinal indigestion the stools are at first 
large and contain an abundance of undigested material and a 
small amount of mucus. Should the disease merge into an 
aitero-colitis, the stool, still large, comes to consist largely of 
mucus and serum and a characteristic cadaveric odor is 
present. The child passes, perhaps, eight or ten stools daily; 
they tend to become smaller and more frequent, and much 
rectal irritation is present. If the mucus is intimately mixed 
with bile, its origin is in the small intestine; if it is clear or 
only streaked with bile, it comes from the lower bowel. Dark 
blood comes from high up in the intestine; bright blood, from 
the lowel bowel; masses of jelly-like mucus, from the rectum 
or lower colon. Cholera infantum is accompanied by serous, 
i. e., watery stools which contain little mucus or food; the 
abdomen is flabby rather than distended, and a hydrocephaloid 
state tends to supervene. (Raue.) 

Prognosis. — Intestinal indigestion generally terminates favor- 
ably in a few days. Entero-colitis runs a course extending 



270 DISEASES OF THE DIGESTIVE SYSTEM. 

over two weeks or more, and without careful treatment tends 
toward a fatal issue. In cholera infantum the outlook is grave, 
death sometimes occurring in twenty-four hours. In any case 
a fall in temperature, a lessened frequency of the pulse, and 
the return of normal constituents to the stool, presages a 
favorable termination. 

Treatment. — In all infantile diarrheas diet is of first import- 
ance. During the acute stages withhold food, giving instead 
barley water, which affords no pabulum for the micro-organ- 
isms present in the intestine. Later, allow carefully selected 
milk, sterilized and diluted with plain lime water. Increase 
the quantity very gradually by adding a little more to the 
barley water each day. Insist upon absolute regularity in the 
hours of feeding. 

In the severe forms remove the poison from the gastro- 
intestinal tract by washing out the stomach, using a soft 
rubber catheter as a stomach-tube, and irrigating the colon 
with clear water. General baths may be used to control pain 
and pyrexia, while a great loss of fluids may demand the use 
of saline solution, a pint or more in twenty-four hours by 
hypodermoclysis. 

In many cases alcoholic stimulation is advisable; add half 
an ounce of brandy, the white of an egg, and a little sugar to 
a tumblerful of water, strain, and administer a teaspoonful 
every hour (Raue). 

In mild cases early febrile symptoms will suggest the use of 
aconite or belladonna, while in the absence of fever mix vomica 
is generally indicated. Later manifestations will be met by 
such remedies as ipecac (nausea, vomiting, green stools), vera- 
trum viride (purging predominating), cuprum ars. (cramps, 
diarrhea), chamomilla (colic, flatulence, fretfulness), and 
podophyllum (thin, copious, painless stools). 

In severe cases arsenic is demanded by choleraic symptoms, 
such as severe vomiting and purging, thirst, restlessness, and 
a tendency to collapse. Croton tig. may be suggested by 
yellow watery stools expelled with great force. Cuprum ars. 



DISEASES OF THE DIGESTIVE SYSTEM. 271 

is valuable in the condition ascribed to arsenic, but with severe 
nervous symptoms and pain. Veratrum alb. is required in 
conditions of impending collapse, the patient being bathed in 
cold sweat. Complete collapse calls for the use of camphor, 
zincum met. or cyanide, or hydrocyanic acid. 

An excess of mucus in the stools suggests the use of mer- 
curius, sulphur, or gummi gntti. 

INTESTINAL OBSTRUCTION. 

(Ileus.) 

Etiology. — Occlusion of the intestinal canal, partial or com- 
plete, may result from a variety of lesions, including the 
following: 

1. Strangulation. The intestine may become constricted 
by inflammatory bands or adhesions, the result of peritonitis; 
or by the forcing of the bowel into pouches, openings, or 
omental or mesenteric slits. 

2. Volvulus. Twists or knots of the bowel are met with 
principally in the large intestine, especially about the sigmoid 
flexure of the colon. Strangulation and volvulus are apt to 
occur in adult males. 

3. Intussusception or invagination. One portion of the 
bowel may slip down into another from above ("telescope"); 
this is particularly common in young children as the result of 
diarrhea or constipation. 

4. Abnormal contents of the bowel. Foreign bodies, such as 
gall-stones, enteroliths, or seeds, may occlude the intestine; 
or fecal impaction, resulting from constipation or from paraly- 
sis of a bowel segment, may produce the same result. 

5. Strictures and tumors. Stricture of the bowel may be 
congenital (imperforate anus) or due to the cicatrices of 
healed ulcers (tuberculous, syphilitic, dysenteric, etc.). It 
may be produced by benign or malignant neoplasms. 

Symptoms. — Acute Obstruction of the intestine is accom- 
panied by: 



272 DISEASES OF THE DIGESTIVE SYSTEM. 

1. Abdominal pain, sudden and severe. 

2. Vomiting. This is apt to be copious, persistent, and 
projectile in character. The vomitus consists first of food, 
then of bile, and finally of fecal matter. This projectile, 
stercoraceous vomiting is pathognomonic of intestinal ob- 
struction. 

3. Constipation. As a rule constipation is absolute from 
the beginning. In a few cases it becomes so only after the 
contents of the intestine below the lesion have been dis- 
charged. 

4. Distention is usually discovered in the bowel above the 
point of obstruction, and it is frequently accompanied by 
visible peristaltic movements of the intestinal coils in the 
same locality. Tenderness is usually diffuse, but it may some- 
times be found localized to the area about the lesion, and 
exceptionally a tumor or stricture may be palpated. Tenes- 
mus is characteristic of intussusception, and may be accom- 
panied by the passage of mucoid and bloody stools. 

5. Collapse usually develops early in the attack. The con- 
stitutional symptoms are profound, but no fever is present 
until peritonitis is set up. 

Chronic Obstruction of the intestines is generally due to 
fecal impaction, foreign bodies, cicatricial strictures, or malig- 
nant neoplasms. Fecal impaction may be diagnosed upon the 
discovery of a rectum filled with hard fecal matter, in addition 
to which a tumor appears sooner or later in the region of the 
cecum. The impaction may be accompanied by attacks of 
diarrhea, the intestinal secretions channelling their way 
through the mass. In cases of chronic obstruction due to 
other causes the symptoms are not characteristic. As a rule, 
there is a history of long-standing constipation, paroxysmal 
abdominal pain, sometimes grooved or .flattened stools, and 
gradual failure in health. Examination usually reveals ab- 
dominal distention, and frequently the peristaltic movements 
of the intestinal coils can be seen through the abdominal 
wall. 



DISEASES OF THE DIGESTIVE SYSTEM. 273 

Diagnosis. — In an acute case the coincidence of sudden severe 
pain in the abdomen, persistent and later stercoraceous vomit- 
ing, constipation, distention, and collapsic symptoms renders 
the diagnosis of intestinal obstruction easy. It is not enough, 
however, to recognize the nature of the lesion; it is essential 
that its character and situation shall, if possible, be deter- 
mined. For this purpose the history, the symptoms, and the 
signs discoverable on physical examination, both external and 
per rectum and vagina, are often necessary. 

Obstruction to the small intestine is usually indicated by the 
sudden onset of intense pain; vomiting is early, copious, and 
persistent; the constipation can be apparently relieved by 
enemata; collapse is common; distention is not marked; and 
indican may be found in the urine. 

Obstruction to the large intestine is less acute in its onset, 
the pain is less severe, distention and constipation are early 
and marked symptoms, and vomiting is delayed and frequently 
scanty. Collapse is a late symptom. Indican is not found in 
the urine. 

Acute general peritonitis may be distinguished by a history 
of one of its causal conditions (appendicitis, pelvic infections) , 
the presence of fever, the characteristic pulse, the more uni- 
form distention of the abdomen, the absence of gurgles in the 
bowel, and the non-projectile character of the vomiting. 

Acute enteritis presents, as a rule, diarrhea and fever, with- 
out marked distention of the abdomen or stercoraceous vomit- 
ing. 

Intestinal colic may be excluded by its history, the character 
and localization of the pain, and the absence of obstinate con- 
stipation, stercoraceous vomiting, collapse, and local tender- 
ness. 

Prognosis. — In the acute form the outlook is extremely un- 
favorable, the disease terminating in death within a week if 
surgery does not intervene. The chronic cases due to fecal 
impaction may terminate favorably through discharge of the 
obstructive mass. Chronic cases due to other causes may be 
18 



274 DISEASES OF THE DIGESTIVE SYSTEM. 

prolonged for weeks, with progressive emaciation and anemia, 
until finally acute obstruction intervenes and death rapidly 
ensues. Surgical measures serve to prolong life in many in- 
stances. 

Treatment. — In cases of acute intestinal obstruction the 
patient should be placed at rest, food withheld, and morphia, 
gr. %, with atropine, gr. T ^o", should be given to control the 
excessive peristalsis. When relaxation has thus been secured, 
the colon may be irrigated with large quantities of warm 
water, in an effort to overcome the obstruction. In some 
cases the patient may be anesthetized and placed in the knee- 
chest position, in order to facilitate the irrigation. Give no pur- 
gatives. If it can be determined that the obstruction is due to 
fecal impaction an enema of oil may be used, as suggested for 
the treatment of constipation. 

Should relief not be secured within twenty-four hours, 
immediate operative interference should be urged. In cases 
of chronic obstruction the treatment should be conducted 
according to the symptoms present and their supposed cause; 
but if the obstruction becomes complete and acute symptoms 
arise, the case must be treated as though it had been acute 
from the start. 

APPENDICITIS. 

Etiology.— The principal cause of appendicitis is the anatomi- 
cal structure of the vermiform appendix itself. This useless, 
feebly-nourished tube, which receives its blood supply from a 
single artery, affords ready ingress to irritating matters, and 
expulsion of the latter is difficult. In women, in whom a 
branch of the ovarian artery affords a more perfect blood 
supply, appendicitis occurs much less frequently than in men. 
Youth, the male sex, intestinal indigestion, exertion (probably 
by causing twists of the appendix), and the presence of foreign 
bodies may predispose to the attack; but the exciting cause 
is invariably bacterial in nature (bacilli coli, streptococci, 
staphlyococci, etc.). 



DISEASES OF THE DIGESTIVE SYSTEM. ZYO 

Pathology. — Inflammations of the appendix may differ in their 
intensity and in the extent of tissue-involvement; and accord- 
ingly the following may be recognized: 

1. Endo-appendicitis . The mucous membrane lining the 
appendix undergoes catarrhal or purulent inflammation; and 
this may result in constriction of the outlet and the formation 
of a retention-cyst, or, occasionally, in adhesion of the walls 
and obliteration of the sac {appendicitis obliterans}. Fre- 
quently, however, this stage is followed by : 

2. Parietal or interstitial appendicitis. The ulcerative pro- 
cess extends, involving all the coats; the swelling constricts 
the tube, and minute abscesses are formed, or gangrene, either 
localized or diffuse, supervenes. This stage invariably ter- 
minates in necrosis or gangrene, with perforation or rupture 
into the peritoneal cavity. 

3. Peri-appendicitis and extra-appendicular lesions. By its 
extension the inflammation leads to: 

(a) Circumscribed peritonitis, either with adhesions between 
the appendix and the adjacent tissues, or the formation of a 
localized abscess. According to the position of the appendix, 
this abscess may point inwards, its rupture leading to diffuse 
septic peritonitis; or it may point inwards and downwards, 
and in that case the pus may rupture into the rectum, bladder, 
or vagina; or it may point upward along the "lateral gutter," 
and if not evacuated it may finally penetrate the diaphragm, 
or the abdominal wall near the umbilicus. Occasionally the 
abscess is retro-peritoneal ("iliac abscess"), and may, finally, 
penetrate in the neighborhood of Poupart's ligament. The 
ileum or the cecum may be involved by the direct spread of 
the appendical inflammation; and occasionally the liver is 
invaded by a thrombus or by septic emboli. 

Diffuse septic peritonitis may directly follow perforation, or 
it may be delayed until the adhesions limiting the latter have 
given way. 

Symptoms. — As a rule the onset of appendicitis is attended 
by a majority of the following symptoms: 



276 DISEASES OF THE DIGESTIVE SYSTEM. 

1. Sudden pain, which may be felt anywhere in the abdo- 
men but tends to localize itself in the right iliac fossa. 

2. Tenderness in the right iliac fossa, especially at Mc- 
Burney's point, two inches from the anterior superior spine of 
the right ilium on a line drawn from that point to the umbilicus. 

3. Rigidity of the right rectus muscle. 

4. Moderate fever and rapid pulse. 

5. G astro-intestinal disturbances. The tongue is coated, 
and vomiting is not unusual; constipation is generally present, 
but diarrhea is not uncommon. 

6. Early there is a tympanitic tumor, reducible by pressure; 
later, if an abscess develops, there will be a hard tumor, also 
tympanitic. 

Varieties. — Appendicitis may be acute, hyperacute, or sub- 
acute in its onset; it may be primary, or may supervene upon 
another disease (typhoid, tubal disease); and it may be 
chronic, either recurring after long intervals of apparent 
recovery during which no tenderness is present, or relapsing 
into a new attack before the previous one has fairly disap- 
peared. 

Course. — Should an attack of appendicitis tend to recovery, 
the pain and rigidity quickly lessen, and in the course of a few 
hours the temperature and pulse-rate fall to normal. Should 
suppuration be present, the temperature usually remains high; 
but either suppuration or gangrene may be unattended with 
fever. 

Should rupture into the peritoneal cavity ensue, it may be 
indicated by a sensation of something having broken in the 
abdomen, followed by severe pain; and the resulting general 
peritonitis will give rise to the following symptoms: 

1. Severe diffuse, not localized, pain. 

2. Uniform distention and tenderness of the abdomen, with 
absence of gurgle. 

3. Moderate fever; sometimes a subnormal temperature. 
\. A rapid, feeble pulse; and a dry, coated tongue. 



DISEASES OF THE DIGESTIVE SYSTEM. 277 

5. Collapsic symptoms: pinched face, hollow eyes, cold, 
clammy skin, feeble pulse, and death. 

Diagnosis. — In typical cases the recognition of appendicitis 
is easy, particularly if the cardinal symptoms of pain, tender- 
ness, and rigidity are kept in mind; but at times a number of 
other conditions may closely simulate the disease. 

Acute intestinal indigestion frequently resembles appendi- 
citis and in fact may usher in the latter disease. The pain of 
indigestion is usually higher in the abdomen, and diarrhea is 
more common than in appendicitis; but the classical symp- 
toms of the latter may develop at any time. 

Acute intestinal obstruction presents no fever, localized 
pain and tenderness are less marked, and vomiting is per- 
sistent and stercoraceous in character. Visible peristaltic 
movements may be observed above the point of obstruction. 

Renal colic is accompanied by pain which extends down the 
ureter and along the spermatic cord, localized tenderness is 
generally absent, and blood or small concretions may be dis- 
covered in the urine. 

Biliary colic is accompanied by pain in the region of the 
gall-bladder and extending toward the umbilicus, tenderness 
is often found over the Mayo-Robson point, and jaundice fre- 
quently appears. 

Perinephritic abscess may simulate appendicitis, but as a 
rule no intestinal symptoms are present, and the history is 
suggestive of chronic renal disease or nephrolithiasis. 

Malignant Disease. — A cancerous mass in the neighborhood 
of the caecum may produce symptoms of obstruction and pain 
strongly suggestive of chronic appendicitis, and frequently 
operation alone can settle the question. 

Floating kidney, by presenting vague pain and a tumor in 
the right side of the abdomen, may resemble chronic appen- 
dicitis; but as a rule the history and physical examination 
will disclose the real nature of the condition. A floating 
kidney predisposes the patient to appendicitis. 

Pelvic affections in women are, as a rule, more gradual in 



278 DISEASES OF THE DIGESTIVE SYSTEM. 

their onset and may be recognized by skillful examination per 

vagi nam. 

Extra-uterine pregna?icy may be distinguished by the men- 
strual history, the lack of fever, and the collapsic character 
of the symptoms which follow rupture; and examination may 
reveal a tumor in the pelvis. 

Typhoid fever is gradual in its onset, and presents a peculiar 
temperature curve and a characteristic eruption at the end of 
a week. Rigidity of the abdominal wall is not prominent in 
typhoid, but in cases attended with early perforation the diag- 
nosis may be very difficult, for it must be remembered that 
appendicitis sometimes develops in connection with typhoid 
fever. 

Prognosis. — While it cannot be doubted that the majority of 
cases of appendicitis will recover without operation, in no case 
can the symptoms be trusted to afford an exact indication as 
to the outcome. Moreover, recurrence is extremely common. 
It is, therefore, difficult to frame a prognosis based solely 
upon the probable results of medical treatment. 

The position and direction of the tenderness afford indica- 
tions of varying gravity, which may be utilized in framing a 
prognosis and determining to what extent treatment may 
venture to be expectant. If the appendix points inward or in- 
ward and upward, it is very dangerous; if inward and down- 
ward into the pelvis, as is usual in women, it is less dan- 
gerous; if outward and upward in the lateral gutter, it is very 
safe (Van Lennep.) 

Should suppuration occur, surgical intervention alone can 
be relied upon to save the patient, although in rare instances 
rupture of the pus into bowel, bladder, or groin has been fol- 
lowed by recovery. General peritonitis renders the prognosis 
almost hopeless. 

Treatment. — As soon as appendicitis is suspected a surgeon 
should be called in consultation and as a rule operation ad- 
vised. Pending this, or when operation is refused, the pa- 
tient should be placed at rest in bed with an ice-bag over the 



DISEASES OF THE DIGESTIVE SYSTEM. 279 

right iliac region, and the large bowel unloaded by means of 
a high rectal enema. If it is certain that suppuration has 
not occurred and the disease is subsiding, a saline purge 
may be given. Opiates must be used only after all questions 
as to diagnosis and treatment have been decided. Liquid foods 
alone are allowable. Early in the attack such remedies as 
belladonna, bryonia, colocynth, cuprum, nux vomica and sul- 
phur may be given; the onset of suppuration calls for mer- 
curius or hepar ; and peritonitis frequently affords indica- 
tions for the use of such medicines as arsenic, cantharis, and 
me r cur. corr. 

CONSTIPATION. 

Etiology. — Constipation may be due to many causes, the 
more important of which are: 

1. Habit, due to a persistent disregard of the natural incli- 
nation to defecation. 

2. Atony of the bowel, with lessened peristalsis; this may 
be due to local disease or general debilitating affections 
(fevers, chlorosis, etc.). 

3. Deficiency of the secretions which normally stimulate 
peristalsis, e. g., bile. 

4. Improper food. Vegetable foods which have a solid 
residue, such as cereals, stimulate peristalsis; but milk, leav- 
ing no residue, has a contrary effect. 

5. Atony of the abdominal walls (over-distention, obesity). 

6. Stricture, due to impingement on the bowel of displaced 
organs (e. g., uterus), tumors, or foreign bodies. 

Treatment. — 1. Ascertain and if possible remove the cause. 

2. Cultivate a regular habit, going to the closet at a certain 
hour each day whether inclined or not. 

3. Adopt a suitable diet; fresh vegetables, fruits, bran or 
gluten bread, and the free use of water between meals. 

4. Massage the abdomen daily. Flex the body repeatedly 
while in the standing position. 



280 DISEASES OF THE DIGESTIVE SYSTEM. 

5. Enemata may be used in obstinate cases. Plain water 
or soap and water may give temporary relief, especially if 
injected into the colon. In very protracted cases with fecal 
accumulation, place the patient in the knee-chest position and 
inject slowly eight or more ounces of olive or cotton-seed oil. 
This should be done by the patient or his attendant at his 
own home and preferably at bedtime; for the patient must 
retain the knee-chest position for twelve minutes, then turn 
gently on to his right side and lie for some hours without 
turning over. This procedure is followed in many instances 
by a thorough emptying of the large bowel and complete re- 
lief of the disorder. 

6. Medicines. Never use a purgative if it can be avoided. 
More useful medicines are mix vomica, suggested by ineffectual 
urging to stool, with headache, nausea, bad taste in the morn- 
ing, and often hemorrhoids, and strychnine, which in atonic 
cases may be substituted for nux. Cases with symptoms of 
portal hyperemia, especially if diarrhea alternates with 
constipation, are benefited by sulphur. Hydrastis is sug- 
gested by sensations of epigastric weakness and sinking, sour 
eructations, hemorrhoids, and hard stools coated with mucus. 
Opium is indicated for the complete intestinal torpor which 
occurs in old people or which follows acute diseases or lead 
colic; the feces are hard and dry. Bryonia may be given when 
similar stools are due to a lack of intestinal secretion, espe- 
cially in irritable hypochondriacs. Many other remedies may 
be suggested by associated symptoms. 

INTESTINAL CANCER 

Intestinal cancer (usually epithelioma, less often colloid 
or scirrhus) is rare. When it does occur it is usually 
primary and in a great majority of cases attacks the rec- 
tum, where it is easily recognizable. It may be annular or 
diffusely nodular. Tumors occurring high up in the intestine 
present no characteristic symptoms; but evidences of chronic 
obstruction of the bowel together with persistent pain and 



DISEASES OF THE DIGESTIVE SYSTEM. 281 

constipation may suggest the nature of the disease, and if in 
addition there are cachexia and altered stools (pus, blood, 
fragments of cancerous tissue) a definite diagnosis is possible. 
Physical examination may reveal a sensitive tumor which does 
not indent on pressure, and which gives a dull tympanitic per- 
cussion note; if it is in the colon or small intestine it is freely 
movable. The prognosis is absolutely unfavorable, although 
surgical measures may prolong life in some cases. 

INTESTINAL NEUROSES. 

1. Secretory. 

Membranous enteritis is a rare disease characterized by the dis- 
charge of a membrane-like substance with the stools. It 
occurs in neurotic individuals, usually women past forty. The 
course is chronic, and treatment should be directed to the 
underlying hysteria or neurasthenia. 

2. Sensory. 

Enteralgia (neuralgia of the bowel) consists of attacks of 
intestinal pain unaccompanied by organic disease of the bowel. 
It may be neurotic or gouty in origin, it may be due to irrita- 
tion of the intestine by its contents, sometimes it is reflex 
from diseases of the other viscera, and occasionally it is due 
to "central causes," i. e., diseases of the brain or spinal cord, 
such as locomotor ataxia or spinal caries. Metallic poisons, 
especially lead, cause severe intestinal pain. The diagnosis 
and treatment should be directed toward the cause, but tem- 
porary relief may often be secured by the use of such symptom- 
atic remedies as colocynth, nux vomica, belladonna, cuprum 
arsen., plumbum, and dioscorea. 

3. Motor. 

Nervous diarrhea may occur as the result of central nervous 
disturbances (c. g., in locomotor ataxia), and in neurotic indi- 
viduals it may be due to emotional disturbances, such as joy 
or fright. A simple increase in the number of stools, without 
change in their consistency, is the usual symptom. 



282 DISEASES OF THE DIGESTIVE SYSTEM. 

DISEASES OF THE PERITONEUM. 

ACUTE PERITONITIS. 

Etiology. — Inflammation of the peritoneum is rarely, if ever, 
primary; as a rule it is secondary to: 

1. Inflammations of the gastro-intestinal tract (perforating 
appendicitis, gastric or intestinal ulcer, toxic gastritis, intes- 
tinal obstruction, strangulated hernia, malignant tumors). 

2. Pyogenic inflammation of the pelvic viscera (puerperal, 
gonorrheal, etc.). 

3. Traumatism (wounds, blows, operative incisions). 

4. Certain general diseases, such as rheumatism and ne- 
phritis. 

Pathology. — As the result of bacterial infection the peri- 
toneum becomes hyperemic and exudation ensues; the latter 
may be: 

1. Fibrinous. The exudate is composed of flakes of yellow 
lymph which tend to glue together the intestinal coils. 

2. Sero- fibrinous. The fibrin produces adhesions and the 
serum gravitates to the flanks. 

3. Purulent. Pus is present in varying, often large, amounts, 
and the inflammation tends to become gangrenous. 

4. Hemorrhagic effusion may occur, especially in cancerous 
and tuberculous cases. 

In extent peritonitis may be: 

a. Circumscribed, the inflammatory process being localized 
by adhesions and virtually constituting an abscess. The latter 
may, however, rupture into the general peritoneal cavity and 
set up diffuse peritonitis. 

b. General or diffuse, the peritoneal surface of the intestinal 
coils being more or less completely covered with a yellowish 
exudate. 

Symptoms. — The onset of acute general peritonitis is sudden, 
and is accompanied by: 



DISEASES OF THE DIGESTIVE SYSTEM. 283 

1. Pain, which is often extremely severe and is rendered 
agonizing by the slightest movement. Its location usually 
corresponds to the area of inflammation. 

2. Tenderness, which is similarly localized. It is so intense 
that in order to relieve the tension of the abdominal walls the 
patient lies on his back with the knees drawn up. 

3. Abdominal distention, due to paralysis of the muscular 
coat of the bowel. This paretic condition leads to consti- 
pation. 

4. Vomiting, at first of the stomach contents and later of 
bile. 

5. A small, rapid, weak pulse. This is characteristic, while 
pyrexia, though usually present, is variable in degree. 

6. Collapse, with cold, clammy skin, pinched face and 
sunken eyes (Hippocratic expression) together with complete 
consciousness and intense mental anxiety. 

Physical Signs. — In addition to abdominal distention and ten- 
derness, the patient may survive long enough for signs of 
effusion to appear, i. e., percussion-dulness and fluctuation 
discoverable first in the flanks and ascending as the amount of 
fluid increases. The gurgling sounds normally heard in the 
intestines are absent and the belly is silent, indicating com- 
plete intestinal paralysis. 

Acute Circumscribed Peritonitis, while presenting these symp- 
toms in milder degree, remains localized; and in addition to 
the pain and tenderness, the fluctuation and percussion-dul- 
ness of an abscess may be recognized. The latter tends, as 
stated, to ultimately rupture into the general peritoneal cavity, 
with fatal results, but it may instead penetrate the stomach, 
bowel, or abdominal wall. 

Diagnosis. — Acute enteritis is accompanied by pain and dis- 
tention, but the pain is colick}', may intermit, is accompanied 
by diarrhea, and severe constitutional symptoms are absent. 

Intestinal obstruction is accompanied by projectile fecal 
vomiting, and lacks extreme tenderness, wiry pulse, and 
pyrexia (until peritonitis supervenes). 



284 DISEASES OF THE DIGESTIVE SYSTEM. 

Hysterical abdomen may resemble peritonitis, but the asso- 
ciated history and conditions, the absence of fever and consti- 
tutional disturbance, and the disappearance of the alleged 
tenderness when the attention is distracted, will usually serve 
to enlighten the attendant. 

In enteralgia the pain is relieved by pressure, fever is absent, 
and the absence of associated conditions serve to render diag- 
nostic confusion improbable. 

Prognosis. — General peritonitis is almost invariably fatal 
within a week. Localized peritonitis may recover through 
surgical intervention, or, rarely, spontaneous discharge out- 
side the peritoneal cavity. 

Treatment. — Abdominal section offers slight hope; but as a 
rule the use of morphine hypodermatically to control pain, ice 
or champagne to relieve vomiting, and liquid food to conserve 
the strength, constitute the main features of the treatment of 
hopeless septic cases. When the peritonitis is circumscribed, 
local applications of cold or heat may aid in checking its 
advance, but surgical interference early in the attack is ad- 
visable. 

In localized peritonitis the early symptoms may be com- 
bated with aconite or veratrum viride, or, in young children, 
belladonna. Upon the development of the characteristic pain, 
bryonia is indicated. Advanced cases with impending heart 
failure may be given arsenic. Intensely septic cases afford in- 
dications for arsenic, cantharis, mercurius corr. , or the snake 
poisons. Typhoid symptoms may suggest the use of rhus 
tox. Failing circulation demands the use of alcoholics or of 
camphorated oil or strychnine hypodermatically. 

Chronic Peritonitis is usually tuberculous, but it may be due to 
cancer, syphilis (in infants), or inflammation of one of the 
abdominal organs involving its peritoneal covering; or it may 
remain as a sequel of an acute attack. The peritoneum may 
become thickened with connective tissue, the intestines may 
be matted together with adhesions, or there may be a varying 
amount of effusion present. Symptoms may result from in- 



DISEASES OF THE DIGESTIVE SYSTEM. 285 

testinal obstruction produced by the adhesions, or there may 
be more or less vague pain; but in many cases no subjective 
evidence of the disease is present. Discovery of the presence 
of fluid in the abdominal cavity may lead to a diagnosis of the 
condition. The treatment should include the administration 
of such remedies as apis, aiiram, kali iod., and sulphur; and 
in many cases repeated paracentesis is necessary. 



ASCITES. 

Etiology. — Abdominal dropsy may result from: 

1. Portal obstruction, either within the liver (cirrhosis) or 
without the liver (thrombosis, or pressure by neoplasms, 
aneurism, peritonitis, etc.). 

2. General venous stasis, due to chronic heart or lung dis- 
ease. 

3. Cachectic states associated with hydremia (anemia and 
nephritis). 

Symptoms. — By its mechanical effect the serous accumulation 
produces abdominal distention with uneasiness and discomfort, 
while pressure upon the veins may cause secondary edema of 
the lower extremities. The latter will, however, precede the 
abdominal accumulation when the dropsy is due to general 
venous stasis. The ascitic fluid is freely movable, and with 
each change of the patient's position it gravitates to depend- 
ent parts. The abdominal viscera may become displaced and 
the diaphragm crowded upward, as a result of which respira- 
tion may be seriously embarrassed. 

Physical Signs. — When the patient stands erect the lower 
portion of the abdomen bulges forward; when he lies down it 
flattens, and the flanks bulge. Placing the hand on one side 
of the abdomen and tapping with the fingers on the opposite 
side, a succussion wave will be felt. By percussion absolute 
dulness is elicited over the fluid, and this dulness alters its 
location with each change of the patient's position. 

Diagnosis. — An ovarian cyst may resemble ascites; but the 



286 DISEASES OF THE DIGESTIVE SYSTEM. " 

cyst is unilateral at first, rises up toward the centre of the ab- 
domen and does not distend the flanks, and the umbilicus 
does not become protuberant as in ascites. Vaginal examina- 
tion may aid the diagnosis. If necessary a small portion of 
the fluid may be withdrawn by the needle; if ascitic, it is gen- 
erally clear and straw colored, with a specific gravity of 1010 to 
1014; if ovarian, it is turbid, of varying color, and its specific 
gravity is 1020 or more. 

Chronic peritonitis with effusion is generally tuberculous. It 
presents some pain and pyrexia, and is usually associated with 
manifestations of tuberculosis elsewhere. If adhesions are 
present the fluid changes its position less readily than in as- 
cites, and on withdrawal it is found to be more albuminous 
and of higher specific gravity than ascitic fluid. 

A distended bladder has been mistaken for ascites, but its 
origin is low in the pelvis and it disappears on catheterization. 

Treatment. — 1. Discover and treat the causal condition. 

2. In severe cases the use of such remedies as apis, arsenic, 
cinchona, helleborus, or iodine is required; or, if these fail, ad- 
minister diuretics, such as infusion of apocynum or of digitalis, 
20 drops every 3 or 4 hours. 

3. Paracentesis should be used only when other measures 
have failed and the condition is extreme. Puncture with a 
straight trocar at a point midway between the symphysis and 
umbilicus, and withdraw the fluid slowly. Use strict anti- 
septic precautions. 



DISEASES OF THE LIVER AND GALL-DUCTS. 

Diseases of the liver may produce many and varied symp- 
toms, both local and general; but as a rule attention is par- 
ticularly attracted to that organ by the occurrence of local 
pain, jaundice, ascites, or dyspeptic symptoms. 

1. Hepatic pain may be felt in the region of the liver, or in 
the right shoulder tip. More often the sensation is one of 
vague discomfort, or a feeling of distention in the right hypo- 



DISEASES OF THE DIGESTIVE SYSTEM. 287 

chondrium calls attention to that region. Intense agonizing 
pain is felt when the bile duct has become occluded, e. g., by 
a stone {biliary colic). 

2. Jaundice is invariably the result of some disease of the 
liver or the gall-passages. The skin, conjunctivae, and mucous 
membranes become uniformly pigmented in shades varying 
from a light yellow to a yellowish green. This icterus is gen- 
erally first detectable in the conjunctiva or in the mucous 
membrane under the tongue. It is accompanied by itching of 
the skin, the urine and saliva are tinged with yellow, and the 
feces are often white from lack of bile. 

3. Ascites, the abdominal dropsy which results from ob- 
struction to the return of blood to the heart by way of the 
portal circulation, is most often due to disease of the liver 
(cirrhosis, etc.). 

4. Dyspeptic symptoms may be of hepatic origin, as the re- 
sult of: 

(a) The absence of bile from the intestine, in consequence 
of which the feces are white in color, and decomposition of the 
intestinal contents takes place, this latter producing flatulence; 
or 

(&) The occurrence of venous stasis in the gastro-intestinal 
circulation, which, by inducing passive congestion and catarrhal 
changes in the mucous membranes, leads to various symptoms 
of irritation in the stomach and intestines. 

Interrogation of the Patient. — When an affection of the liver is 
suspected, careful inquiry should be made as to: 

1. A history of dietetic errors, alcoholism, gastric catarrh, 
previous attacks of jaundice, companionship with dogs (echino- 
coccus), syphilis, prolonged suppuration (amyloid degenera- 
tion), or exposure to poisons, especially phosphorus. 

2. Pain. What is its location ? Has he ever had an attack 
of severe pain coming on suddenly and lasting for some hours ? 
Did the pain at that time radiate, and if so, in what direction ? 
Was there vomiting with it ? Was he yellow afterwards ? 
Does he ever have pain in the tip of his shoulder? 



288 DISEASES OF THE DIGESTIVE SYSTEM. 

3. Jaundice. Has he noticed any change in the color of his 
skin, his urine, or his feces? Does his skin itch? 

4. Venous stasis. Is his abdomen swollen ? Does he suffer 
with piles ? Has he ever vomited blood ? Does he suffer with 
gastro-intestinal symptoms, such as epigastric discomfort, dis- 
tention, belching, constipation, etc.? 

Examination of the Patient. — Inspection of the hepatic region 
may reveal nothing of importance. In some cases, however, it 
may be noticed that the abdominal veins have become dilated 
and prominent, or even varicose and serpiginous in the neigh- 
borhood of the umbilicus (caput Medusa), thus indicating the 
establishment of collateral avenues to compensate for portal 
obstruction. A localized edema may be noted (abscess of the 
liver), the hepatic region may be diffusely elevated (hepatic 
hypertrophy), or an isolated pyriform swelling may be ob- 
served in the middle of the epigastrium (dilated gall-bladder). 
Rarely the lower margin of the liver can be seen moving up 
and down with respiration. On inspection we may also dis- 
cover pulsations in the liver (heart disease). 

Palpation. — Place the patient on his back with the ab- 
dominal walls relaxed, distract his attention with conversa- 
tion, and place one hand flatly on the abdomen, just outside 
of the rectus muscle. Depress the side of the hand slightly 
so as to push up a fold of skin and ask the patient to take a 
deep breath; as he does so the margin of the liver may be 
felt to ride over the edge of the hand. If this method is un- 
successful, place the left hand against the right lumbar region 
and endeavor to press the liver upward, while the right hand 
makes gentle continuous pressure and gradually works down 
so as to reach the border of the liver. If the examiner is in 
doubt as to whether he really feels the edge of the liver, let 
him search for the fissure of the gall-bladder, or for that near 
the median line produced by the round ligament. 

In health the liver is rarely palpable, but when increased in 
size, as the result of hyperemia, obstruction in the gall-ducts, 
inflammation, syphilis, malignant disease, fatty infiltration, or 



DISEASES OF THE DIGESTIVE SYSTEM. 289 

amyloid degeneration, the organ may extend several finger- 
breadths below the border of the ribs. The surface of the 
liver may be felt to be granular (cirrhosis), or nodular (carci- 
noma), and its edge may be smooth and rounded (amyloid 
disease). In cases of enlargement due to circulatory, inflam- 
matory, or degenerative processes which involve the organ as 
a whole, the normal shape is usually preserved, and this may 
serve to exclude such conditions as cancer, abscess, or hydatid 
cyst. The liver, and consequently tumors attached to it, 
move with respiration. 

By palpation the degree of pain can be ascertained. Pain 
accompanies disease of the liver only when its peritoneal cov- 
ering is inflamed (perihepatitis, syphilis, cancer) or rapidly 
distended (hyperemia, abscess, hydatid cyst). Pain is also 
the result of irritation of the gall bladder or ducts. Peri- 
hepatic friction is sometimes felt over the liver. It consists 
of a peculiar sensation like the creaking of leather, com- 
municated to the examiner's hand and also heard during 
auscultation; it is produced by the rubbing together of the 
roughened hepatic and parietal layers of the peritoneum. 
The hydatid thrill is a sensation like that felt on percussing a 
bladder filled with water. To elicit it, place the left hand on 
the tumor and note the vibration produced by percussing in its 
neighborhood with the right hand. The hydatid thrill is not 
invariably present in echinococcus cysts, and it is also met in 
connection with ovarian cysts and even simple ascites. Pal- 
pation may also reveal morbid conditions of the gall bladder; 
the latter cannot be detected unless distended, when it may 
be felt as a smooth, pear-shaped tumor, extending out toward 
the umbilicus. It may be enlarged, soft, and fluctuating 
(dropsy), or it may contain gall-stones and impart a sensation 
like that felt on squeezing a bag of marbles. 

Percussion. — In order to permit percussion of the liver an- 
teriorly, the patient should lie on his back, but for percussion 
posteriorly he must stand, sit, or lie on his left side. The 
normal limits of dulness are as follows: 

19 



290 



DISEASES OF THE DIGESTIVE SYSTEM. 



Upper 
border. 



fDeep percus- 

!sion-dulness 
(use forcible 
percussion). 
I Superficial per. 
cussion - dul- 
L ness. 



r 

tower border (use light | 
percussion and pass up- "I 
wards). 



Median Line. 



I Blends with 
J- heart dul- 
ness. 



Mammary 
Line. 



4th inter- 
space. 



6th rib. 



A hand's 
breadth be-; | About the 
low the base| \ costal mar- 
of the xiph- j gin. 
oid. I 



Mid-axillary 
Line. 



? th interspace, 



8th rib. 



J ioth inter- 
J space. 



Scapular Line. 



9th interspace. 



ioth rib. 



\ Blends with 
>- kidney dul- 
) ness. 



MALFORMATIONS AND MALPOSITIONS OF THE LIVER. 

Malformations. — Alterations in the shape of the liver may be 
congenital or acquired. Syphilis may produce a lobulated 
liver which pathologically presents the changes of a chronic 
interstitial hepatitis; and the symptoms are those of the latter 
disease. The " corset liver," in which a furrow across the an- 
terior and lateral surface is produced by compression, is very 
common in women, but occasions no direct symptoms. In 
some of these cases careful palpation along the edge of the 
liver may be necessary in order to distinguish the lower por- 
tion from an abdominal tumor. 

Malpositions. — The liver may be transposed, appearing mainly 
on the left side. This is usually associated with transposition 
of the other viscera. It may be displaced in various direc- 
tions, as the result of tight lacing, or by the pressure of 
pleuritic effusion, emphysema, ascites or abdominal tumors. 
The " wandering liver " which is permitted by an abnormally 
long suspensory ligament to fall out of its usual position, gen- 
erally occurs in middle-aged women with lax abdominal walls 
{splanchnoptosis} . The organ may be recognized as a large, 
hard, movable tumor, corresponding in shape and size to the 
liver, while the normal site of the latter is tympanitic on per- 
cussion. Various dragging sensations and nervous symptoms 
may be induced by the displacement. The treatment is 
limited to the application of an abdominal supporter. 



DISEASES OF THE DIGESTIVE SYSTEM. 291 



CIRCULATORY AFFECTIONS OF THE LIVER. 

Anemia of the liver occurs in connection with a general 
anemia, or with fatty or amyloid degeneration of the organ, 
but it occasions no symptoms and is discovered only post 
mortem. 

Active Hyperemia (congestion) of the liver takes place physio- 
logically after each meal, and it may be exaggerated by in- 
dulgence in rich food or alcohol, and may even eventuate in 
interstitial changes. It also accompanies malaria and other 
infectious diseases, and suppression of menstruation. It 
causes no characteristic symptoms. 

PASSIVE HYPEREMIA OF THE LIVER. 

Etiology. — Passive hyperemia of the liver results from obstruc- 
tion of the flow of blood from the liver. Its cause may be: 

1. Local, such as pressure over the portal area from with- 
out (by a tumor or cyst), venous thrombosis, etc. 

2. General, especially in connection with the venous stasis of 
uncompensated heart disease, less often as the result of chronic 
pleurisy, emphysema, and intra-thoracic tumors. 

Pathology. — The central vein of each lobule and its adjacent 
capillaries become congested, and by contrast with the paler 
periphery of the lobule, an alternation of tints is produced 
which is recognized post mortem as the "nutmeg live?'." 
Later, atrophy is induced, the central cells and capillaries 
being replaced with dark pigment and connective tissue {red 
or cyanotic atrophy). 

Symptoms. — The liver becomes enlarged and tender, and its 
lower edge can be detected considerably below the border of 
the ribs. The patient complains of discomfort in the right 
hypochondrium, together with such gastro-intestinal symp- 
toms as a furred tongue, nausea, vomiting, diarrhea, or consti- 
pation. There may be slight jaundice or ascites, or general 
anasarca may be present. Congestion of the gastric mucous 



292 DISEASES OF THE DIGESTIVE SYSTEM. 

membrane, hyperemia and enlargement of the spleen, and 
congestion of the kidneys, in consequence of which the urine 
is scanty and of high specific gravity, are more or less con- 
stantly associated with hyperemia of the liver as results of the 
same general condition, i. e., venous stasis. 

Treatment. — This must be directed to the causal condition, 
most frequently heart disease with broken compensation. In 
many of these cases digitalis and other heart tonics fail to act 
until the dropsy and portal stasis have been removed, and the 
latter may be accomplished by the administration of mercuriu's 
dulcis, lx, in doses of one grain every two or three hours for 
several days. 

PERIHEPATITIS. 

Etiology. — Inflammation of the peritoneal covering of the 
liver may result from: 

1. The spread by continuity of a hepatic inflammation (ab- 
scess, hydatid cyst). 

2. Perforation of the stomach or intestine (ulcer, appen- 
dicitis, etc.). 

3. The spread of pleurisy through the diaphragm. 

4. Direct violence, such as a blow, or continued pressure. 

5. General peritonitis. 

Pathology. — The inflammation may be plastic, a fibrinous 
exudate leading to the formation of adhesions, but more often 
it is purulent, the space between the liver and the diaphragm 
becoming filled with circumscribed areas of pus {.subdiaphrag- 
matic or subphrenic abscess). Air or gas derived from the 
lung or gastro-intestinal tract may also be present {subphrenic 
pyopneumothorax) . In a more chronic form of perihepatic 
inflammation the capsule becomes thickened and attached by 
adhesions to adjacent organs, and ultimately the liver itself 
becomes shrunken and its vessels and ducts occluded. 

Symptoms. — In acute cases the onset is attended with the 
circumscribed pain and tenderness characteristic of a localized 



DISEASES OF THE DIGESTIVE SYSTEM. 293 

peritonitis, while rigors and irregular pyrexia may announce 
the formation of an abscess. During the early stage a friction 
rub may be heard over the hepatic area, and when an abscess 
has formed the right hypochondrium becomes distended, the 
intercostal spaces appear motionless, the line of percussion 
dulness is elevated, and the lower border of the liver is de- 
pressed. 

Course. — The duration is extremely variable; if the exudate 
is fibrinous, resolution may occur in a few days; but if the 
process is purulent the disease may be prolonged, death finally 
resulting from asthenia or rupture of the abscess into a neigh- 
boring organ. Rarely the pus is absorbed or is evacuated 
through the abdominal wall, and recovery follows. 

Diagnosis. — Empyema of the right pleural cavity may be 
distinguished by the presence of cough and expectoration, and 
the displacement of the heart to the left. If there be doubt, 
aspirate in the seventh or eighth interspace in the midaxillary 
line; the presence of bile pigment in the pus, sometimes suffi- 
cient in amount to render the latter very yellow, indicates the 
subdiaphragmatic location of the abscess. 

Prognosis. — The fibrinous variety terminates favorably in a 
short time. In the absence of surgical interference the puru- 
lent cases generally prove fatal. 

Treatment. — In an acute case it is essential that the patient 
be placed at rest and his suffering controlled by hot fomenta- 
tions and opiates if necessary. Aconite may be given at the 
outset, but as the local inflammation develops, bryonia or 
asclepias is usually indicated. Rhus tox. may be given in 
cases resulting from traumatism, and sulphur in those whose 
course is protracted. Hepar, mercurius, or silica may be 
administered when suppuration occurs, but at the same time 
appropriate surgical measures become necessarv. 

ABSCESS OF THE LIVER. 

(Suppurative Hepatitis.) 

Etiology. — Suppuration within the liver is due to the pres- 
ence of pyogenic micro-organisms, the sequence of: 



294 DISEASES OF THE DIGESTIVE SYSTEM. 

1. Traumatism, either by external injury, or by foreign 
bodies, or parasites (echinoccoci). 

2. Infection through the portal vein. This may follow 
intestinal ulceration (especially dysentery), rectal operations, 
abdominal abscess, or infectious diseases of the portal vein 
itself (suppurative pylephlebitis). 

3. Infection through the hepatic artery, (pyemia, septic 
emboli). 

4. Infection through the umbilical vein, due to infection of 
the navel in the new-born. 

5. Infection through the bile-duct, a sequel of cholangitis. 

6. Infection from adherent adjacent organs, such as an 
ulcerated or cancerous stomach. 

Certain cases in which the infection cannot be traced are 
classed as idiopathic. Adult males are most frequently at- 
tacked. 

Pathology. — The abscess may be single, as in the tropical 
(amoebic) variety, or multiple, as in pyemic cases. In a 
majority of cases the right lobe of the liver is affected. The 
abscess may penetrate the diaphragm and lung, it may burrow 
into the peritoneal cavity, into the pericardium, into the 
adjacent abdominal viscera, or through the abdominal wall 
externally. If rupture does not occur and life is preserved, 
encapsulation may take place. 

Symptoms. — The abscess may be unsuspected, the symptoms 
resembling those of typhoid (high fever, delirium, tympanites, 
enlarged spleen, and even a roseolous eruption), of malaria, 
(quotidian intermittent fever), or tuberculosis (cough, dyspnea, 
emaciation, anemia, night sweats, etc.). As a rule, however, 
tenderness and pain may be discovered in the hepatic region, 
and often pain is felt in the shoulder-tip. The fever is septic 
in type, often high (104-105°), and accompanied by chills and 
sweats. Jaundice is not usual. The liver may be enlarged 
upward, and as suppuration progresses, fluctuation may be 
detected. 



DISEASES OF THE DIGESTIVE SYSTEM. 295 

Diagnosis. — An abscess ma}* be overlooked for a time, though 
the possibility of its occurrence should be suggested by a his- 
tory of dysentery, gall-stone colic, injury about the liver, or 
residence in the tropics. Tuberculosis may be excluded by 
examination of the lungs and sputum; malaria, by examina- 
tion of the blood, which presents leucocytosis and no Plas- 
modium; and pleural effusion, by the diminished fremitus and 
resonance which are found over the area of dulness. Hepatic 
intermittent fever, due to an impacted calculus, offers a his- 
tory of biliary colic, together with more marked jaundice and 
less grave general symptoms. A hydatid cyst ma}- require 
aspiration for the discovery of its character. In doubtful cases 
the patient should be anesthetized and the exploring needle 
used, with antiseptic precautions. 

Prognosis. — This is generally unfavorable, although evacua- 
tion of the abscess and free drainage has greatly reduced the 
mortality. Multiple pyemic abscesses are invariably fatal. 

Treatment. — Support the patient's strength with nourishing 
liquid food and stimulants. Baptisia, belladonna, Bryonia, 
Jiepar, lacJiesis, mercury, or quinine arsenite may be indicated 
in the early stages, but when evidences of suppuration are 
present the abscess must be opened and drained. 



CIRRHOSIS OF THE LIVER. 

Etiology. — The term "cirrhosis" comprises a group of dis- 
eases which have as a common feature the development of 
fibrous tissue within the liver. The causes may be: 

1. Toxic, i. e., poisons taken as food or drink or as medi- 
cinal agents (alcohol, spices, etc.). 

2. Infective, the source of the infective agents being local 
(.inflammations of the stomach, intestinal, or bile passages) or 
general (malar'a, scarlatina, etc.). 

It is probable that various irritants by setting up a gastritis 
lead to the formation of toxins in the stomach or intestines. 
The latter are absorbed into the portal circulation, and carried 



296 DISEASES OF THE DIGESTIVE SYSTEM. 

to the liver, where, they induce chronic inflammatory changes, 
either by their own direct action, or indirectly by destroying 
the resistance of the liver to the action of certain micro- 
organisms. 

Syphilis causes a special form of hepatic cirrhosis. The 
liver may also become involved in the general sclerotic 
changes of senility; and fibrosis often follows long-continued 
passive congestion. 

Pathology. — The liver may be enlarged {hypertrophic) or 
diminished in size {atrophic), the latter frequently represent- 
ing the terminal stage. The organ is hard and the cut surface 
appears yellowish, brownish, or mottled. The newly-de- 
veloped fibrous tissue may form a coarse net-work which 
permeates the whole organ and encloses in each mesh a num- 
ber of lobules {.mult i lobular or Laennec s cirrhosis), or a finer 
network of connective tissue, in which a plexus of bile ducts is 
imbedded, may surround single lobules {uni lobular or biliary 
cirrhosis). In another form the connective tissue penetrates 
the lobules themselves, surrounding single cells or groups of 
cells {intra-lobular or peri-cellular cirrhosis), and in a fourth 
variety dense bands of cicatricial tissue traverse the liver 
irregularly and by their contraction produce considerable 
deformity of the organ {gummatous or syphilitic cirrhosis). 
As a result of the pressure induced by these changes the 
nutrition of the secreting cells of the liver is interfered with, 
and they undergo progressive degeneration. In the course 
of time the contraction of the connective tissue leads to ob- 
struction of the portal circulation, and ascites results. 

Symptoms. — The disease is gradual in its onset and occasions 
no characteristic symptoms until obstruction to the portal 
circulation has induced congestion of the stomach and intes- 
tines. The first symptoms, therefore, are dyspeptic in char- 
acter; the patient complains of anorexia, eructations of gas, 
distention, gastric discomfort, and constipation. As the portal 
obstruction increases, ascites develops, and the dropsical ac- 
cumulation often becomes enormous. Hemorrhoids are usually 



DISEASES OF THE DIGESTIVE SYSTEM. 297 

present. As the gastrointestinal symptoms increase in sever- 
ity, hemorrhages may take place from the stomach or bowels, 
and sometimes from the esophagus or nose. In an attempt to 
form a collateral circulation, the venous channels of the abdo- 
men dilate and the surface becomes marked with varicose 
veins, notably around the umbilicus, where their ramifications 
may produce the so-called caput Medusa. Jaundice is rarely 
present, but the skin is nearly always sallow, and the patient 
becomes emaciated. Edema of the legs is a late symptom, 
due to the pressure of the ascitic accumulation upon the blood 
returning from the lower extremities. The urine is scanty, 
high-colored, and loaded with bile pigment and urates. 
Toward the close of the disease toxemic symptoms, such as 
drowsiness, coma, or delirium, may supervene. 

Hypertrophic Cirrhosis — Enlargement of the liver, while 
often representing merely an early stage of cirrhosis, may in 
some cases be accompanied by no tendency to contraction. 
Such cases are distinguished by early and deepening jaundice, 
by absence of gastro-intestinal irritation and of ascites and other 
symptoms of portal obstruction, and by the presence of ten- 
derness over the liver. The urine is bile-stained and the urea 
is normal in amount. The course of the disease is often rapid, 
terminating with toxemic symptoms (coma or delirium) within 
a year or two. 

Diagnosis. — In the early stages diagnosis is very difficult. The 
disease often remains unsuspected until ascites or gastro- 
intestinal hemorrhage leads to examination of the liver. If in 
the absence of acute disease or starvation that organ is found 
to be reduced in size, and especially if the spleen is enlarged, 
cirrhosis may be inferred. It is essential that the liver be 
examined after the ascitic accumulation has been removed 
and meteorism reduced, for the presence of either of these 
conditions causes an apparent diminution in the size of the 
organ. 

Chronic peritonitis y with its liquid effusion, may be mis- 
taken for the abdominal dropsy of cirrhosis, but in the former 
there is abdominal tenderness, the liver is not diminished in 



298 DISEASES OF THE DIGESTIVE SYSTEM. 

size, and the fluid obtained by paracentesis is apt to be turbid 
and to contain matters suegestive of its inflammatory origin. 

Hypertrophic cirrhosis may be confused with cancer of the 
liver, but the latter is not accompanied by splenic enlarge- 
ment, the organ is usually nodular, and ascites is infrequent. 
Amyloid disease may be accompanied by splenic enlargement 
but not by jaundice. Enlargement of the liver may be asso- 
ciated with chronic biliary obstruction, but generally there is a 
history of recurrent attacks of colic and transient jaundice, 
and the spleen is not enlarged. 

Prognosis. — As a rule the prognosis is unfavorable. The 
course of the disease extends over many years, but, unfor- 
tunately, ascites and the other symptoms due to portal ob- 
struction, by which it is often first recognized, occur only as 
terminal events. Even at this period life may be much pro- 
longed by judicious treatment. Should the disease be dis- 
cerned earlier in its course, the outlook is more favorable. 
The hypertrophic stage is, therefore, sometimes amenable to 
treatment. 

Treatment. — The cause, whether it be alcohol, or syphilis or 
some other infection, must if possible be discovered and re- 
moved. In order to reduce the activity of the liver, the 
patient should be placed on an exclusive milk diet. Only 
when the patient absolutely refuses to submit to this restriction 
is it advisable to permit other foods; and in such a case fats, 
sugars, and starches should be avoided and preference given 
to the proteid foods. The gastric catarrh should receive 
attention; in particular, the patient should sip a glassful of 
hot, preferably alkaline, water before each meal in order to 
free the stomach of mucus. 

The early symptoms, which are principally gastro-intestinal, 
will afford indications for such drugs as argentum nit., arsenic, 
cinchona, iris, lycopodium, mercnrius, mix vomica, and podo- 
phyllum. Small doses of mercnrius are recommended by 
physicians of all schools. Later, the appearance of ascites 
and the evidence of portal obstruction may lead to the se- 
lection of aurum, iodine, or phosphorus. Potassium iodide is 



DISEASES OF THE DIGESTIVE SYSTEM. 299 

highly commended by many authorities, and is of undoubted 
value in cases of syphilitic origin. 

As the disease progresses, purgatives and diuretics may be 
used to lessen the abdominal stasis. Mercurius dulcis, lx, in 
grain doses every two or three hours, is often of great service 
at this stage. Digitalis, half a drachm or more of the in- 
sion every three hours, caffein, gr. iv, three times a day, theo- 
bromine, gr. v-x, t. i. d., may be used. Ultimately, however, 
paracentesis becomes necessary for the removal of the ascitic 
accumulation, and since the latter re-accumulates rapidly the 
operation may have to be repeated many times. After empty- 
ing the bladder with a catheter, introduce a trocar at a point 
in the median line midway between the umbilicus and the 
pubis. Withdraw the fluid slowly, and when the latter ceases 
to flow, remove the canula, cover the wound with adhesive 
plaster, and apply an abdominal binder. Under strict anti- 
sepsis the operation is free from danger. 

Notable amelioration of the symptoms due to portal ob- 
struction maybe secured by surgical means. The parietal peri- 
toneum and the omentum are scarified and then sutured to- 
gether, and in this way anastomatic channels sufficient for 
collateral circulation are provided. 

AMYLOID DEGENERATION OF THE LIVER. 

(Lardaceous, albuminoid, or waxy liver.) 

Etiology. — Amyloid degeneration of the liver, like amyloid 
disease of other organs, is usually the result of prolonged sup- 
puration, notably that incident to tuberculosis, or of syphilis. 
Less often it is associated with cancerous and other cachexias. 

Pathology. — The liver is enlarged, often enormously, but pre- 
serves its normal shape and smoothness. On section the 
tissue appears waxy and stains a mahogany brown with a 
watery solution of iodine. Similar changes are found in the 
other viscera, particularly the kidneys and the spleen. 

Symptoms. — The degeneration occasions no characteristic 
symptoms, neither jaundice nor portal obstruction ensuing. 



300 DISEASES OF THE DIGESTIVE SYSTEM. 

The patient complains of sensations of enlargement and 
weight in the hepatic region, and he becomes anemic, and 
finally dropsical. The associated amyloid change in the kid- 
neys occasions the characteristic signs of that lesion. 
Diagnosis. — The diagnosis rests upon the following data: 

1. A history of the conditions favoring amyloid degenera- 
tion (prolonged suppuration, tuberculosis, syphilis, etc.). 

2. An enlarged, firm, smooth liver, which is not tender. 

3. An associated cachexia and often dropsy. 

4. Evidences of amyloid degenerations in other organs. 
Prognosis. — Should the causal condition be removable, the 

degenerative process in the liver may be arrested. In general, 
however, the amyloid change is progressive and terminates in 
the course of a few years in death. 

Treatment. — Treatment must be directed to the primary dis- 
ease. The suppurative lesion may be controlled by surgi- 
cal means, the medicinal treatment being directed to the as- 
sociated symptoms. Syphilitic cases should receive appropriate 
remedies, the more important of which are ciicrum, mercury, 
and potassium iodide. 



ACUTE YELLOW ATROPY OF THE LIVER. 

(Acute parenchmatous hepatitis; malignant jaundice; icterus gravis. ) 

Etiology. — The exciting cause of this rare and fatal disease is 
unknown, although it is probably a violent toxin, perhaps au- 
togenetic or infective in its origin. The disease occurs more 
often in middle-aged,women and rather frequently during preg- 
nancy. Pre-existing infectious diseases and alcoholic and 
other excesses seem to predispose to it. A similar lesion may 
be produced by the toxic action of arsenic, antimony, or phos- 
phorus. 

Pathology. — The liver becomes small, its capsule is wrinkled, 
and microscopically the cells appear disintegrated into fat 
droplets and granules or crystals of bile pigment. The kid- 



DISEASES OF THE DIGESTIVE SYSTEM. 301 

neys undergo parenchimatous inflammation, and the other 
viscera show degenerative changes. 

Symptoms. — 1. Prodomal stage. The early symptoms are 
those of gastro-intestinal irritation, including anorexia, nausea, 
vomiting, and prostration. Jaundice appears in a few days, 
beginning about the face and neck and extending over the 
whole body. 

2. Stage of full development. In the course of a few days 
the prostration becomes more intense and the jaundice more 
marked, the skin even assuming a greenish hue. The tem- 
perature rises, and grave nervous symptoms — headache, deli- 
rium, convulsions, stupor, and coma — develop. Hemorrhages 
ma}' arise from the skin or mucous membranes. At first the 
liver seems to be enlarged, but it rapidly diminishes in size 
and in a few days its dulness may be discoverable only in the 
axillary line. The urine is concentrated, deeply bile-stained, 
and slightly albuminous; the amount of urea is diminished, 
and casts, leucin, and tyrosin are present. The spleen is en- 
larged. 

Diagnosis.— In the prodromal stage the disease cannot be dis- 
tinguished from ordinary catarrhal jaundice, but the nervous 
symptoms, ecchymoses, hepatic atrophy, and urinary changes 
of the later stage render a diagnostic error improbable. PJios- 
plioriis-poisoning is accompanied by vomiting, violent gas- 
tralgia, and diarrhea, nervous symptoms are less pronounced, 
and leucin and tyrosin are not found in the urine. In phos- 
phorus-poisoning a remission of three or four days follows the 
gastro-intestinal symptoms and precedes the appearance of 
jaundice. Phosphorus ma}' be discovered in the stomach con- 
tents. Yellow fever may be distinguished by its geographical 
localization, and by its sudden invasion, which is accompanied 
by general pains, black vomit, and high fever. 

Prognosis. — Death almost invariably occurs, generally within 
two weeks, as the result of cholemia or uremia. 

Treatment. — A milk diet, cold water enemata, and the admin- 
istration of phosphorus are advisable. Special symptoms may 
afford indications for other remedies. 



302 DISEASES OF THE DIGESTIVE SYSTEM. 

FATTY LIVER. 

Varieties. — An accumulation of fat in the cells of the liver 
may occur in two forms, viz., 

1. Infiltration of the cells with fat drops, which simply push 
the protoplasm to one side and thus by preventing its nutrition 
may ultimately cause its disappearance {fatty infiltration) . 

2. Metamorphosis of the cell protoplasm itself into fat, with 
consequent impairment of its function and ultimately complete 
cell disintegration {fatty degeneration). 

Fatty infiltration of the liver may be due to : 

(1) Over-ingestion of fats, which are stored in the liver; or 

(2) Diminished oxidation, notably that attendant upon 
anemic and cachectic states, which permits the fat to accumu- 
late unchanged in the liver. This is particularly common as a 
result of alcoholism and of pulmonary tuberculosis. 

The fatty liver becomes greatly enlarged, smooth, and pale, 
and the microscope exhibits hepatic cells containing large 
drops of fat. Outside of the physical condition, which may 
be ascertained by palpation and percussion, the disease pre- 
sents no characteristic symptoms. The liver can be completely 
restored to its normal state by control of the causal condition; 
otherwise, its unfavorable influence on digestion and general 
nutrition may hasten death from other causes. 

Fatty degeneration of the liver is a grave disease, probably 
always toxic in origin, as a result of which the individual cells 
become degenerated and destroyed and the liver undergoes a 
reduction rather than an increase in size. The process, exam- 
ples of which are seen in phosphorus-poisoning and acute 
yellow atrophy, is uncontrolled by treatment and invariably 
ends in death. 

CANCER OF THE LIVER. 

Etiology. — Carcinoma of the liver is usually secondary to 
cancerous growths of other organs, especially those related to 
the liver by the portal circulation. As a rule, though not 



DISEASES OF THE DIGESTIVE SYSTEM. 303 

always, it attacks individuals who have reached middle or ad 
vanced life. 

Pathology. — Cancer of the liver occurs chiefly in two forms 
viz., 

1. The nodular form. Multiple nodules, gra} T ish white in 
color and varying in number from three or four to several 
hundred, are scattered through the substance of the organ, 
and may be felt upon its surface, even through the abdominal 
wall. Degeneration and absorption of the central cells of the 
nodule may be followed by contraction which leads to an um- 
bilication of its centre. 

2. The diffuse form. A general cancerous infiltration of the 
liver sometimes occurs and as a result the organ becomes en- 
larged in all its diameters. 

Less frequently the cancer is radiating in form, and rarely it 
is colloid. In a few cases it is engrafted on a pre-existing 
cirrhosis and in consequence the liver becomes slightly if at 
all enlarged. Degenerative changes may lead to hemorrhages, 
and the extravasated blood may burst into the gall-bladder or 
peritoneal cavity. Occasionally suppuration occurs around a 
nodule. 

Symptoms. — The patient shows signs of ill health; he com- 
plains of loss of strength and some tenderness or pain in the 
region of the liver, his appetite is poor and his digestion im- 
paired, and he rapidly becomes emaciated and cachectic. 
Jaundice is present in nearly one-half of the cases, as the re- 
sult of obstruction to the bile ducts. Ascites is infrequent, oc- 
curring only when the portal vein or its branches become 
obstructed by the growth. Physical examination reveals en- 
largement of the liver, which is often enormous; and fre- 
quently it is possible to palpate the superficial nodules and 
even their central umbilications. 

Diagnosis. — In the presence of a recognized primary growth 
elsewhere the hepatic neoplasm may for a time escape obser- 
vation, but ultimately attention will be directed to the liver 
and its enlargement noted. Advanced age, rapid emaciation, 



304 DISEASES OF THE DIGESTIVE SYSTEM. 

hepatic tenderness, and the presence of either jaundice or 
ascites afford strong presumptive evidence of hepatic cancer. 
Fatty infiltration and amyloid degeneration are distingished 
by their history and by the absence of malignant symptoms 
and of jaundice. Multilocular echinococcus cysts are rare; 
they fluctuate, and are associated with splenic enlargement. 
Tumors of adjacent organs do not move with respiration. An 
enlarged gall-bladder is pear-shaped, and its situation is 
lower. 

Neoplasms other than carcinoma, especially sarcomata, 
may involve the liver, but they correspond so exactly in both 
clinical course and prognosis that differentiation is unnecessary. 

Prognosis. — The disease is invariably fatal, usually within a 
year. 

Treatment. — Symptomatic and palliative. 

JAUNDICE. 

(Icterus.) 

Etiology. — Staining of the tissues and fluids of the body with 
bile pigment is a symptom, not a disease. It is usually due 
to obstruction of the bile-ducts, the result of: 

1. Catarrhal inflammation and swelling of the mucous mem- 
brane lining the duodenum or the ducts (catarrhal jaundice). 

2. Foreign bodies (gall-stones, parasites) within the ducts. 

3. Stricture or obliteration of the duct. 

4. Tumors obstructing the duct from within. 

5. Pressure on the duct from without (enlarged glands in 
the hilum of the liver, tumors of the adjacent viscera, displaced 
organs, fecal accumulations, cicatrices, gravid uterus, abdomi- 
nal aneurism). 

6. Lowered blood pressure in the hepatic circulation favor- 
ing resorption of the bile, as in the simple icterus of the new- 
born. 

In addition to the above obstructive causes, the jaundice 
resulting from which has been termed hepatogenous, a second 



DISEASES OF THE DIGESTIVE SYSTEM. 305 

variety of icterus has been ascribed to non-obstructive causes, 
such as widespread necrosis of the liver cells or increased 
destruction of the blood cells (yellow fever, phosphorus-poison- 
ing, etc.), and termed hematogenous. The propriety of this 
distinction is questioned. 

Symptoms. — 1. Cutaneous symptoms. The jaundice appears 
first on the sclerotic or upon the mucosa of the mouth, espe- 
cially when the latter is rendered temporarily anemic by press- 
ure, and then upon the skin, first at its thinnest parts. The 
shade of yellow varies, and marked changes in its hue may be 
noticed from day to day. The patient is tormented with itch- 
ing of the skin, which is apt to be worse at night. Erythema- 
tous or bullous eruptions, and if the disease be of long-stand- 
ing, xanthelasma, may be associated; and in cases of grave 
icterus there may be ecchymoses. 

2. Intestinal symptonis. Failure of the bile to reach the 
intestine (acholia) leads to lessened digestive activity and fat- 
absorption. The lack of bile wherewith to precipitate the 
pepsin from the chyme permits that substance to destroy the 
pancreatic ferment, and as a result the digestion of proteids 
and carbohydrates is also hindered, and general nutrition 
suffers accordingly. The patient is usually constipated, and 
putrefaction of the intestinal contents leads to gas-formation 
and consequent meteorism. The tongue is coated, there may 
be anorexia, nausea, and vomiting, and the feces are whitish 
and contain an excess of undigested fat. Less commonly an 
excess of bile pours into the intestine {polycholia) causing a 
dark coloration of the stools and perhaps a biliary diarrhea. 

3. Secretory symptoms. Bile-pigments change the color of 
the urine to a yellow or brown which becomes greenish on 
exposure to the light. Albumin and casts may be present. 
The perspiration, the sputum, and even the breast milk may 
be more or less stained with bile. In any secretion its pres- 
ence will be revealed by Gmellin's test. (See page 201.) 

4. Symptoms of auto-intoxication. Various toxic phenomena 
may be observed. The pulse is slowed (40-50), the patient is 

20 



306 DISEASES OF THE DIGESTIVE SYSTEM. 

depressed in spirits and often irritable, progressive emaciation 
is apt to ensue, and such grave nervous symptoms as delirium, 
convulsions, tremors, and the typhoid state may appear. The 
temperature is lowered, and visual disturbances are not un- 
common. 

Diagnosis. — The sallow skin of general ill-health must not be 
mistaken for jaundice; it is usually an anemia and is not 
accompanied by straining of the conjunctiva and the secre- 
tions. Addison s disease presents a brownish discoloration 
which is more marked on exposed portions of the body and 
does not stain the sclerotic or the urine. 

It is not enough, however, to recognize the existence of 
jaundice; diagnosis implies discovery of the cause and seat of 
the obstruction. Acute jaundice is usually due to catarrh of 
the common duct; if there is fever, the smaller ducts are in- 
volved. If the gall-bladder is distended and palpable, it sug- 
gests obstruction of the common duct, and if it is painful and 
tender, the obstruction is probably a gall-stone. The paler 
the feces, the more complete the obstruction and the more 
probable its seat in the common duct; for with obstruction of 
the cystic duct, bile still enters the intestine; and with obstruc- 
tion of the hepatic duct, bile continues to flow until the gall- 
bladder is emptied and the jaundice is not associated with 
distention of the gall-bladder. Persistent jaundice indicates 
organic liver disease or permanent outside obstruction. 

Prognosis. — This depends entirely upon the cause. 

Treatment. — That of the causative condition. 

ICTERUS NEONATORUM. 

Diffuse jaundice is not unusual in new-born children, and 
two forms are recognized, the first of which is similar to ordi- 
nary obstructive jaundice and disappears in a week or two, 
while the second is usually fatal. This grave variety may be 
due to absence of the hepatic or common duct, to congenital 
syphilitic hepatitis, or to septic phlebitis of the umbilical vein. 
Treatment is unnecessary in the first variety and useless in 
the second. 



DISEASES OF THE DIGESTIVE SYSTEM. 307 



SIMPLE CATARRHAL JAUNDICE. 

Etiology. — Jaundice may be due to catarrhal inflammation of 
the common duct, not the result of an impacted gall-stone, 
and the local catarrhal condition may be caused by: 

1. Local infection, the exciting cause of which is unknown. 
The disease may be epidemic. 

2. Extension of an inflammatory process from the duode- 
num (gastro-intestinal disorders). 

3. Infectious diseases elsewhere, especially pneumonia, ty- 
phoid fever, etc. 

Pathology. — The mucous membrane of the duct becomes 
greatly swollen and its lumen may be occluded with mucus. 

Symptoms. — 1. Jaundice, with yellow skin, dark urine, and 
pale stools. 

2. Gastro-intestinal derangements, with anorexia, nausea, 
vomiting, constipation, etc. 

3. Slight fever may be present. 

Diagnosis.— The appearance in a young adult of jaundice un- 
accompanied by pain or emaciation, especially if there is a 
history of pre-existing gastro-intestinal catarrh or other causa- 
tive condition, usually justifies a diagnosis of catarrhal jaun- 
dice. Exceptionally it is necessary to exclude acute yellow T 
atrophy, cancer, or cirrhosis. 

Prognosis. — Favorable, recovery usually being completed 
within three weeks. 

Treatment. — The patient should be placed at rest in bed and 
his diet limited to milk, beef broths, egg albumin, and an 
abundance of plain or saline water. Warm baths and weak 
solutions of carbolic acid may be used to relieve the itching of 
the skin. 

The more important remedies, which are usually indicated 
by the gastro-intestinal symptoms, are cJielidonium, cinchona, 
colocynth, hydrastis, kali bichromicum, mercuriits, mix vomica, 
and podopJiyllin. 



308 DISEASES OF THE DIGESTIVE SYSTEM. 



CHOLELITHIASIS. 

(Gall-Stones; Biliary Lithiasis; Biliary Calculi.) 

Etiology. — At least two-thirds of the cases of cholelithiasis 
occur in women, usually those past 40 years of age. Irregular 
meals, the excessive ingestion of carbohydrates and fats, 
tight-lacing, constipation, pregnancy, and the gouty diathesis 
have been named as predisposing causes. Most of these are 
conditions which interfere with the free flow of the bile, caus- 
ing its retention in the gall-bladder or ducts. In addition, a 
catarrhal inflammation extending into the gall-ducts may par- 
tially occlude the passage with mucus and desquamated 
epithelium, thus slowing the current of bile. As a result, 
cholesterin, bile-pigments, and salts of lime and magnesia are 
precipitated about a nucleus composed of epithelium or mucus, 
and a gall-stone is formed. These calculi may vary in size 
from a grain of sand to a peach, and in number from a single 
one to several thousand; they range in color from yellow to 
brown or green, and are apt to be irregularly faceted. 

Course. — 1. The stone may remain latent in the gall-bladder 
or ducts. 

2. The stone may pass oat through the ducts; in that case 
its passage may or may not be accompanied by severe pain 
{biliary colic). 

3. The stone may become impacted: 

(a) In the cystic duct, causing distention of the gall-bladder 
with a thin mucoid fluid {.dropsy, hydrops vesica fellece) or 
with pus {empyema, suppurative cholecystitis). Ulceration 
and perforation may ensue. 

{b) In the common duct, causing obstructive jaundice, 
biliary colic and sometimes intermittent fever. 

4. The stone may ulcerate through into the peritoneal 
cavity, the adjacent viscera, or through the abdominal wall 
externally. 

5. The stone may become impacted in the intestine, caus- 
ing obstruction. 



DISEASES OF THE DIGESTIVE SYSTEM. 309 

Symptoms. — 1. Calculi in the gall-bladder may exist for an 
indefinite time without producing symptoms. In some cases 
the patient complains of occasional attacks of discomfort, 
tenderness, or pain in the hepatic region, with reflex digestive 
disturbances and sometimes slight fever. 

2. The passage of calculi through the ducts may, if the 
stones are small, give rise to no symptoms; but the larger 
calculi occasion an attack of biliary colic severe in proportion 
to the size of the stone and the degree of obstruction which it 
causes. Biliary colic is characterized by a sudden attack of 
excruciating pain which centres in the right hypochondrium 
and is accompanied by nausea, vomiting, and often cold sweat 
and collapsic symptoms. If the stone is in the common duct 
the typical tenderness at the Mayo-Robson point, with pain 
radiating thence to the umbilicus, will be present. In half of 
the cases jaundice appears, usually within '24 hours. The 
duration of the attack varies from a few hours to a week or 
more. Symptoms of chronic obstruction may follow. 

3. (a) Obstruction of the cystic duct may be caused by 
cicatrices or neoplasms as well as gall-stones. Physical ex- 
amination may reveal some rigidity of the muscles in the right 
hypochondriac region, with sensitiveness or pain which is 
more marked when a deep breath is taken. Careful palpation 
usually discloses the smooth, oval, distended and fluctuating 
gall-bladder. Jaundice never results from obstruction of the 
cystic duct alone. Dropsy of the gall-bladder or an acute 
infectious inflammation of the gall-bladder {acute cholecystitis) 
may ensue. It is accompanied by paroxysmal pain in the 
right hypochondrium, nausea, vomiting, and more or less 
prostration; and suppuration {suppurative cholecystitis, em- 
pyema of the gall-bladder), gangrene, and perforation may 
result. Cholecystitis ma}' also follow an acute infectious dis- 
ease, notably pneumonia or typhoid fever, After an attack 
of the latter disease its specific organism is found quite con- 
stantly in the biliary passages. 

{b) Obstruction of the common duct may be due to the 
presence of foreign bodies, cicatrices, or to compression from 



310 DISEASES OF THE DIGESTIVE SYSTEM. 

without, as well as to gall-stones. The symptoms vary with 
the cause. When it is an impacted gall-stone, occlusion of 
the outlet leads to biliary colic. A stone in the common duct 
produces tenderness at a point two-thirds of the way from the 
tip of the ninth costal cartilage to the umbilicus (Mayo-Rob- 
son point), and the pain runs from the point toward the um- 
bilicus. More or less jaundice is present. Should the impac- 
tion persist, a catarrhal cholangitis arises and is accompanied 
by fever of an intermittent type (Charcot's, or hepatic, ijiter- 
mittent fever) which strongly resembles malaria in its recur- 
rent paroxysms of chill, fever, and sweat. In a few cases the 
cholangitis becomes suppurative, and as a result the fever is 
more septic in type and leads to death. 

4. Perforation of the gall-tracts may be the result of in- 
fective gangrene or pressure-necrosis induced by the stone. 
Perforation into the peritoneal cavity will be followed imme- 
diately by symptoms of general septic peritonitis. The symp- 
toms of penetration into the gastro-intestinaj tract are very 
obscure and a diagnosis is rarely possible unless intestinal 
obstruction occurs. Occasionally free bile in the stools will 
suggest the possibility of such an occurrence. Perforation in- 
to the urinary tract may be indicated by the appearance of 
large quantities of bile, cholesterin, or hepatic calculi in the 
urine. The thoracic cavity may be invaded by a hepatic ab- 
scess which penetrates into the pleural cavity or lung, or the 
pus may burrow from the gall-bladder into the subphrenic 
space or mediastinum without involving the liver, ultimately 
rupturing into the pleura or lung; in the latter case the symp- 
toms are those of septic pleurisy. A biliary fistula may pene- 
trate the abdominal wall and discharge externally ; usually it 
follows the course of the round ligament and appears at the 
umbilicus. 

5. Impaction of a gall-stone in the intestine will give rise to 
symptoms of intestinal obstruction (q. v.). As a rule a stone 
large enough to become impacted in the bowel will first have 
ulcerated through from the gall-duct. 

Diagnosis. — In the absence of distinctive symptoms the diagno- 



DISEASES OF THE DIGESTIVE SYSTEM. 311 

sis of cholelithiasis may be difficult. Great significance should 
be attached to a history of attacks of colic, of recurrent 
jaundice, or of an intermittent fever, especially if typhoid, 
tuberculosis, and malaria can be excluded. Careful physical 
examination may detect a distended gall-bladder or other 
evidences of the lesion. Tenderness at the Mayo-Robson 
point accompanied by pain running from that point to the 
umbilicus is strong presumptive evidence of a stone impacted 
in the common duct. Obstructive jaundice arising in the 
common duct and accompanied by enlargement of the gall- 
bladder almost invariably means cancer. Obstructive jaundice 
thus arising without distention of the gall-bladder, almost 
always indicates a stone. (Van Lennep). Following a sus- 
picious attack of colic, for several days the fecal discharges 
should be washed on a sieve in order to secure the positive 
evidence afforded by discovery of the stone. 

Gastralgia usually occurs in neurotic individuals; the pain 
is referred to the stomach and back; it occurs when the 
stomach is empty, is relieved by eating, and fever and jaundice 
are absent. 

Renal colic starts in the flank and the pain radiates down 
the ureter; the testicle of that side is painful and often re- 
tracted, and the urine may be scanty and blood-stained. 

In intestinal colic the pain usually centres about the umbili- 
cus and is relieved by firm pressure; often there is flatulence, 
and neither jaundice nor the stone can be discovered sub- 
sequently. 

Prognosis. — Attacks of biliary colic usually terminate favor- 
ably; but the prognosis as to complete recovery must be 
guarded. If the inflammatory conditions are limited to the 
gall-bladder, if it is possible to remove all stones and to break 
up adhesions, perfect recovery may be assured; but generally 
this is possible only through surgical intervention. 

Treatment. — During a paroxysm of biliary colic some relief may 
be obtained from the application of heat and the administration 
of symptomatically indicated remedies {belladonna, calcarea 



312 DISEASES OF THE DIGESTIVE SYSTEM. 

carb., nux vomica)', but since the cause of the pain is essen- 
tially mechanical, only an opiate can be expected to afford 
decided relief. Morphine, gr. %, with atropine, gr. tto> may 
be given hypodermatically, and in aggravated cases inhalations 
of chloroform may be necessary. Evidences of persistent im- 
paction, the development of dropsy or empyema of the gall- 
bladder, or suppurative symptoms of any kind justify surgical 
intervention. The surgical procedure in cases of cholelithia- 
sis consists of removal of the calculi, followed by drainage or 
irrigation of the biliary passages to cure the catarrh. 

When the attack has subsided, the patient should be placed 
on a diet free from alcohol, fat, sugar, and starch. He should 
live an active open-air life as far as possible; and if a pro- 
longed visit to Saratoga or Bedford Springs is impossible, he 
should be ordered to drink one quart of water, containing 
from one to three drachms of Carlsbad Spriidel salt, daily. 
Medicines should be selected in accordance with the indica- 
tions present; the more important are calcarea carb., cheli- 
donium, cinchona, lycopodiiim, nux vomica, and sulphur. 

Cancer, either primary or secondary to carcinoma of the liver 
or other adjacent viscera, may have its seat in the gall-bladder 
or gall-ducts. In addition to such general symptoms as ema- 
ciation and cachexia, evidences of biliary obstruction are 
usually present. 

Stenosis of the common duct may be due to ulceration arising 
during the passage of a gall-stone, subsequent inflammatory 
adhesions completely occluding the duct. It may also be 
caused by external pressure, such as that of a tumor. Ob- 
structive jaundice results. 

Parasites (echinococcus, distoma hepaticum, etc.) may cause 
obstruction by their entrance into the larger biliary passages. 
The symptoms do not differ from those of hepatic obstruction 
due to other causes, except in cases where the presence of the 
echinococcus gives rise to a hydatid cyst. 



DISEASES OF THE DIGESTIVE SYSTEM. 313 



DISEASES OF THE PORTAL VEIN. 

Thrombosis of the portal vein {adhesive pylephlebitis), though 
rare, may result from traumatism, cirrhosis, cancer, external 
pressure, or retardation of the blood current; it is probable 
that a roughened venous wall is essential to the formation of 
the thrombus. It may occur in an} 7 portion of the portal 
tree, may be either partial or complete, and if organization of 
the clot ensues the vessel becomes transformed into a fibrous 
cord. Symptoms may be absent if the thrombosis is limited 
to portions of the hepatic vessels; if it is extensive, the sudden 
obstruction leads to the signs of venous stasis, i. e., ascites, 
gastro-intestinal disorders, and hemorrhages. Jaundice is 
unusual. Hepatic cirrhosis can be excluded by a history of a 
sudden onset and the absence of atrophy of the liver. If the 
obstruction is limited to one of the smaller branches of the 
veins, an efficient collateral circulation may become estab- 
lished; but if the larger branches are occluded, the ultimate 
prognosis is highly unfavorable. The treatment should be 
that recommended for cirrhosis of the liver. 

Septic thrombosis of the portal vein {.suppurative pylephlebitis) is 
usually secondary to suppurative inflammations of the intes- 
tines (gastric ulcer, appendicitis, typhoid fever, dysentery) or 
to abdominal abscesses. Rarely it may be due to perforation 
of the portal vein by a foreign body (<?. g., a swallowed fish 
bone), and in new-born children it may follow septic infection 
of the umbilicus. Septic emboli are washed into the liver, 
where they lodge upon the walls of the larger vessels or within 
the minute hepatic branches and give rise to multiple ab- 
scesses. The symptoms are those of (1) abscess of the liver, 
together with (2) portal obstruction, and (3) general septi- 
cemia or pyemia. The condition is hopeless, and treatment 
can be only symptomatic or palliative. 



314 DISEASES OF THE DIGESTIVE SYSTEM. 



DISEASES OF THE PANCREAS. 

Diseases of the pancreas are by no means common, and even 
when they are present the accompanying symptoms are so 
obscure that their recognition is often extremely difficult. There 
may be discomfort or actual pain deep in the epigastrium, and 
should the solar plexus be implicated the pain may become 
severe and agonizing, radiating in every direction. Disturb- 
ance of the secreting function of the gland may lead to deficient 
pancreatic digestion, with fatty stools as a result. In such 
stools the fat appears as solid masses, white or yellow in color; 
sometimes it is liquid at the body temperature, and becomes 
solid on cooling after ejection. Glycosuria is frequenty the re- 
sult of serious degenerative or destructive lesions of the pan- 
creas. 

The head of the pancreas is in close relation posteriorly to 
the common bile duct, the inferior vena cava, and the portal 
vein; and in consequence pancreatic tumors in that situation 
may press upon the bile duct, causing persistent jaundice, or by 
pressure upon the blood vessels it may bring about edema and 
ascites. Pyloric or duodenal obstruction may be induced in 
the same way. 

Physical examination of the pancreas is very difficult, owing to the 
depth at which the organ lies in the epigastrium behind the 
stomach. Under normal circumstances it is completely out of 
reach, and only raeely do morbid changes render it more 
accessible. With the stomach and colon empty and the 
abdominal walls relaxed, deep palpation may sometimes 
enable the examiner to detect a tumor at a point about mid- 
way between the umbilicus and the ensiform appendix, which, 
in the presence of suspicious symptoms, may be attributed to 
the pancreas. 

ACUTE PANCREATITIS. 

Etiology. — The cause of this rare affection is practically un- 
known. It occurs oftenest in men over thirty, a few of whom 



DISEASES OF THE DIGESTIVE SYSTEM. 315 

are alcoholic and many of whom have previously suffered with 
gastro-intestinal disorders. It may originate in a pancreatic 
hemorrhage induced by traumatism. 

Pathology. — The pancreas becomes swollen and infiltrated 
with blood. White spots of fat necrosis may alternate with 
hemorrhagic foci, and the hemorrhagic effusion may involve 
the peri-pancreatic tissues and the mesentery {hemorrhagic 
pancreatitis). 

Gangrene often follows these hemorrhagic extravasations, 
either the tip or the entire gland becoming softened and 
necrotic '{gangrenous pancreatitis). 

In some cases the lesion becomes purulent instead of gan- 
grenous, and as a result the organ contains one or many small 
abscesses {suppurative pancreatitis). Localized peritonitis 
and thrombosis of the splenic and portal veins may ensue. 

Symptoms. — The patient is suddenly attacked with severe 
and deep-seated pain in the epigastrium, and this is followed 
by vomiting, abdominal distention, and constipation. There 
is tenderness in the epigastric region, often a subnormal tem- 
perature, and usually the patient dies within three days. 
Should he survive longer, gangrenous changes may supervene, 
and are accompanied by chills, fever, sometimes jaundice, and 
finally collapse and death. Rarely life is prolonged oyer three 
or four weeks, and during that time irregular chills and a septic 
temperature may indicate that a suppurative process is in 
progress. 

Diagnosis. — Acute intestinal obstruction generally occurs in 
the lower portion of the tract, is often accompanied by visible 
peristalsis of the intestinal coils and by fecal vomiting, often 
projectile in character; and it lacks the localized epigastric 
pain and tenderness of pancreatitis. Irritant poisoning may 
be excluded by the history, and by examination of the mouth 
and the vomitus. Intestinal or gastric perforation is almost 
always preceded by symptoms of ulceration. Perforation of 
the gall-tracts usually follows symptoms of cholelithiasis, the 
pain and tenderness are in the region of the gall-bladder, and 
jaundice is common. 



316 DISEASES OF THE DIGESTIVE SYSTEM. 

Prognosis. — The disease is exceedingly fatal, death usually 
occurring within a week. 

Treatment. — The treatment is largely palliative. Shock may 
be combated by the use of external heat, stimulants, and saline 
infusions. Symptoms may suggest the administration of 
arsenic, belladonna, iris, mercurius, or phosphorus. Surgical 
interference may be considered. 

Chronic Pancreatitis, an intestinal fibrosis as the result of which 
the organ becomes hardened and the secreting structure 
atrophied and degenerated, is frequently found in connection 
with diabetes mellitus. In the absence of glycosuria it pre- 
sents no characteristic symptoms. Associated digestive dis- 
turbances may afford indications for various remedies. 

Pancreatic calculi may result from the precipitation of the 
inorganic constituents of the pancreatic juice. Pancreatic 
colic may accompany their passage through the duct. The 
symptoms of the latter resemble those of biliary colic, but the 
pain usually radiates to the left, and jaundice occurs only in 
those rare cases in which the calculus, becoming impacted 
near the orifice, presses upon the common bile duct. A posi- 
tive diagnosis is, however, almost impossible, and the treat- 
ment must be symptomatic. 

Pancreatic cysts arise from obstruction of the duct by calculi, 
cicatricial contraction, or pressure from without. The result- 
ing retention-cysts may be single or multiple, and contain a 
viscid alkaline fluid. No symptoms present themselves until 
the objective evidences of an abdominal tumor appear. The 
latter is situated in the epigastrium or left hypochondrium, 
and is smooth, globular, and resistant. It may be difficult to 
distinguish it from other abdominal tumors. If aortic aneurism 
can be excluded, aspiration should be made. The fluid ob- 
tained from a pancreatic cyst is frequently capable of emulsi- 
fying fats and converting starch into sugar. The treatment is 
surgical. 

Cancer of the Pancreas usually begins in the head of that organ, 
but its further course may involve the entire gland, converting 



DISEASES OF THE DIGESTIVE SYSTEM. 317 

it into a symmetrical tumor; or it may be scattered through 
the organ in the form of cancerous nodules. The symptoms 
include digestive disorders, dull pain in the epigastrium, ema- 
ciation, and cachexia. The stools may be fatty, glycosuria 
may be observed, and obstruction to the common bile duct 
frequently causes jaundice. The disease usually proves fatal 
within a year. As a rule, the treatment is either symptomatic 
or merely palliative. Operation may be considered, however. 



DISEASES OF THE SPLEEN. 

Most of the morbid conditions of the spleen are associated 
with diseases of the blood, and its remaining lesions are, as a 
rule, secondary to disorders of other organs. Occasionally, how- 
ever, attention is attracted to the latter by subjective or ob- 
jective signs originating in the spleen. Enlargement of that 
organ may give rise to sensations of dragging weight in the 
left hypochondriac region (malaria, leucocythemia) or its rapid 
increase in size may exert traction on its own interstitial frame- 
work and thus cause pain. Pain may also result from inflam- 
mation of its peritoneal covering {perisplenitis). 

Examination of the Spleen, — With the patient recumbent, lay 
the hand flat on the abdomen so that the finger tips, pushing 
up a fold of skin, lie close to and under the left costal margin at 
the 10th cartilage. If the spleen is greatly enlarged its edge can 
then be felt. If it is not, press forward with the other hand, 
placed posteriorly about the 10th rib, and let the patient take 
a deep breath; the sharp edge of the spleen, moving with 
respiration, can then be felt to ride over the fingers. 

In order to percuss the spleen, have the patient carry his 
left arm up over his head. Then begin at the costal margin 
and percuss along the 10th rib until dulness is found; this 
represents the anterior border of the spleen, and normally it 
should be in the mid-axillary line. Percuss again from a point 
midway between the posterior axillary and scapular lines 
downward until resonance becomes impaired; this represents 



318 DISEASES OF THE DIGESTIVE SYSTEM. 

the upper border of the spleen, normally about the 9th rib. 
Percuss along the 10th rib from the spinal column out- 
wards; normally splenic dulness occurs about V/z inches from 
the median line, but it is difficult to determine exactly. Per- 
cuss from below the border of the ribs in the posterior axillary 
line in order to outline the lower border of the spleen; nor- 
mally it is just above the costal margin. 

The area thus outlined is normally an oval a trifle more 
than 2 by 3 inches in size. Clinically, it is sufficient to deter- 
mine the vertical diameter; if it exceeds 3J4 inches, enlarge- 
ment of the spleen may be at least suspected, but the diagnosis 
is not positive unless the lower edge is palpable. 

The spleen becomes more or less acutely enlarged in con- 
nection with almost all of the acute infectious diseases. A 
chronic enlargement accompanies malaria, leucocythemia, 
splenic anemia, pernicious anemia, and amyloid disease; and 
it may result from portal congestion due to either cardiac or 
hepatic obstruction. The spleen may become displaced down- 
ward by a pleural effusion, emphysema, or a thoracic tumor. 
It may be pushed upward by tympanites or ascites. A float- 
ing spleen, recognizable by its shape, its notched edge, and its 
mobility, may be encountered in the abdominal cavity. (See 
sp la n ch n op tos is . ) 

Splenitis may be the result of traumatism, or it may be due 
to extension of inflammation from an adjacent organ, such 
as the stomach, diaphragm, or lungs. It is accompanied by 
tenderness and enlargement of the organ. 

Splenic Abscess occurs in connection with pyemic processes; 
it may rupture into the gastro-intestinal tract, the peritoneal 
cavity, or the lung. 

Rupture of the Spleen may result from traumatism or from a 
sudden intense hyperemia of the organ, such as occurs in a 
pernicious malarial fever. It occasions sharp pain in the left 
hypochondrium, speedily followed by collapse and death. 

Neoplasms of the Spleen are usually gummatous; occasionally 
carcinoma, sarcoma, or tuberculosis involves the organ; and 
a hydatid cyst is possible. 



DISEASES OF THE DIGESTINE SYSTEM. 319 

Amyloid Spleen is indicated by the discovery of a hard, smooth 
enlargement of the organ, associated with amyloid degeneration 
of other organs and a history of its causative conditions. 

Floating Spleen may be discovered as a movable hard tumor 
of characteristic shape in the abdominal cavity. It should be 
restored to its place and retained there, if possible, by ex- 
ternal support (see splanchnoptosis'). 



DISEASES OF THE BLOOD. 



Attention may be directed to the condition of the blood by 
pallor of the skin and mucous membranes, associated with 
more or less physical weakness. The blood changes of which 
these symptoms are indicative may be primary {essential 
anemia), but in a great majority of cases they are secondary, 
i. e. , symptomatic of one of those visceral diseases which are 
accompanied by wasting {e. g. t tuberculosis, carcinoma, etc.). 
Only when the latter can be excluded is the diagnosis of a 
specific blood disease made possible by examination of that 
fluid, but since certain general diseases also lead to more or 
less characteristic hemic changes, a knowledge of the latter is 
frequently essential for purposes of differential diagnosis. 

CLINICAL EXAMINATION OF THE BLOOD. 

By examination of the blood we ma} 7 determine: 

(1) The existence or non-existence of a condition of anemia, 
and if the latter be present, its type and severity. 

(2) The existence or non-existence of leucocytosis, and if 
that condition exists, its type and extent, including the recog- 
nition of leucocythemia. 

(3) The presence or absence of blood parasites, including 
those pathognomonic of malaria, nlariasis, and relapsing fever. 

(4) The existence of definite serum reactions, such as the 
Widal test for typhoid fever. (See page 30.) 

(5) The presence of bacterial organisms. For the identifi- 
cation of the latter, culture methods are necessary. 

The practical examination of the blood includes investiga- 
tion of each of the following details: 

1. The macroscopic appearance of the blood. 
21 



322 DISEASES OF THE BLOOD. 

2. The microscopic appearance of the blood, including — 

(a) The appearance of the fresh blood. 

(b) The appearance of the stained blood. 

(c) The enumeration of the corpuscles. 

(3) The estimation of the amount of hemoglobin. 

To secure a specimen of blood, cleanse and dry the finger tip or 
the lobe of the ear, and prick it with a sharp needle or guarded 
lancet-point deep enough for the blood to exude of its own 
accord — pressure must not be used. Wipe away the first 
drop. The second and succeeding drops may be secured, as 
will be directed, for the various steps of the examination. 

1. Macroscopic appearance of the blood. 

Freshly shed blood appears to the naked eye as a homo- 
geneous red fluid, which after a varying period of time sepa- 
rates into serum and clot. In certain pathological states 
(e. g. y hemophilia) it may be important to ascertain the time 
required for this coagulation to take place. For a rough 
clinical test, allow a few isolated drops of blood to fall on a 
glass slide. Draw a fine clean needle through one drop after 
another at short but regular intervals, and note the time which 
elapses before a filament of fibrin, drawn out from the drop by 
the needle, indicates beginning coagulation. More accurate 
results may be obtained by the use of Wright's coagulation 
tubes. 

2. Microscopic appearance of the blood. 

(a) Examination of the fresh blood tinder the microscope. 

Touch the exuding drop, with the cover-glass and imme- 
diately place the latter face down upon the slide, without 
exerting undue pressure. The specimen may be ringed with 
vaseline to prevent rapid drying out. Observe: 

(1) The shape of the red corpuscles {erythrocytes}. 

Normally, under the microscope they appear disc-shaped 
with a central depression. Their contour is unaltered in 
chlorosis and other mild anemias, but in severe anemias they 
may appear to be distorted (poikilocytes), abnormally small 
(microcytes), or abnormally large {macrocytes}. 



DISEASES OF THE BLOOD. 323 

(2) The tendency to rouleaux formation. 

This disappears when the number of red corpuscles is ex- 
cessively diminished, as in some anemias. 

(3) The number of red corpuscles. 

This can be determined accurately only by use of the count- 
ing apparatus, but the practiced eye will quickly recognize 
any great diminutition in their number. 

(4) The color of the red corpuscles, normally yellow, may 
become notably pale, especially in cases of chlorosis. 

(5) The number of white corpuscles, especially in proportion 
to the red. Normally there is one white to about five hundred 
red. This proportion becomes greatly increased (leucocytosis) 
in many diseases, and in some cases, especially in those of 
leucocythemia, this change may be discovered at a glance. As 
a rule, however, the counting apparatus is necessary. 

(b) The examination of the stained blood under the micro- 
scope requires the preparation of films. For this purpose, 
allow a drop of blood to fall upon a clean, dry cover-glass and 
cover it with another glass, and then separate them by gently 
sliding one over the other. Or, allow the drop of blood to 
touch the surface of a perfectly clean slide and use the edge of 
another slide, held at an angle of about 45°, to spread the 
drop evenly along the slide. The films must be made quickly, 
before the corpuscles can become altered, and must be as 
uniform and as thin as possible. After allowing them to dry 
in the air, place the films for five minutes or more in a mixture 
of equal parts of absolute alcohol and ether, and then stain them 
from two to eight minutes in Ehrlich's triple stain; or, stain 
them first in an alcoholic solution of eosin for about half a 
minute, wash, and counter-stain with Delafield's hematoxylin 
solution (freshly filtered) for fifteen seconds or more. Wash 
in clean water, clear with xylol, and if a permanent prepara- 
tion is desired, mount in Canada balsam. Then place one under 
the microscope, and search for — 

(1) Nucleated red corpuscles ("blasts"). These are present 
in the blood during intra-uterine life, but appear after birth 



324 DISEASES OF THE BLOOD. 

only in connection with grave forms of anemia, and in leu- 
cocythemia. As regards size, they may be normal {normo- 
blasts}, abnormally small (microblasts) or abnormally large 
(me galo blasts). These normoblasts and megaloblasts may be 
distorted in shape (poikiloblasts). 

(2) The different forms of white corpuscles. These are dis- 
tinguished according to the character of their nuclei, as 

a. Small mononuclear leucocytes, somewhat less in diameter 
than a red corpuscle, with a single large nucleus which occu- 
pies nearly the whole of the cell, and stains deeply with 
hematoxylin. Normally they constitute about 25% of the 
total number of leucocytes. 

b. Large mononuclear leucocytes, often two or three times the 
size of a red corpuscle, with a large oval nucleus which stains 
but faintly with hematoxylin. They constitute about 6% of 
the leucocytes. A form in which the nucleus becomes in- 
dented, or horse-shoe-shaped, has been termed transitional. 

c. Polynuclear leucocytes (neutrophiles), larger than the red 
cells, are characterized by several nuclei connected by threads 
so as to resemble one irregular nucleus. They constitute 65 
to 70% of the leucocytes. This is the variety chiefly present 
in pus, and they are supposed by their action as phagocytes to 
protect the organism against bacterial invasion. 

d. Eosinophile cells are large, round, and nucleated, and are 
characterized by glistening granules which become deeply 
stained by eosin. They constitute not over 2-4% of the 
leucocytes in normal blood. 

e. Myelocytes (Markzellen). — Unlike the other leucocytes, 
these forms are never found in normal blood. They are large 
bodies, from three to seven times the diameter of a red cor- 
puscle, and have an extremely pale nucleus lying in the centre 
or to one side of the cell. They differ from the large mono- 
nuclear or transitional forms in their much greater size and in 
the pallor of the nucleus. 

The leucocytes may be also differentiated, on the basis of 
their staining reaction with a triple stain, into: 



DISEASES OF THE BLOOD. 



325 



a. Basophiles, cells taking a blue stain in their protoplasm. 

b. Neutrophils, cells taking a lilac stain in their proto- 
plasm. 

c. Oxyphiles, cells taking a golden-red stain in their proto- 
plasm. 

Of the leucocytes, 20-25% are basophiles, 60-75% are neu- 
trophils, and >^-5% are oxyphiles. 

A differential count of the leucocytes is made by counting, say, 
five hundred or one thousand and classifying them according 
to the variety of their nuclei. This serves to indicate whether 
each is present in its normal proportion. 

(r) The enumeration of the corpuscles. 

(1) Counting the red corpuscles. For this purpose the 
Thoma-Zeiss apparatus is used. Place the point of the small 




Fig. 23. — Thoma-Zeiss pipette. . 

pipette in a drop of fresh blood as it exudes from the puncture, 
and suck gently on the rubber tube until the blood exactly 
reaches the point marked 1; then quickly wipe the outside of 
the pipette with a clean cloth, to remove an} 7 adherent blood, 
and immerse the tip in the diluting fluid (Gower's solution, 
consisting of sodium sulphate, grs. 104; acetic acid, 3j; and 
distilled water, 3iv. ) and suck until the latter reaches the mark 
101. While doing this roll or shake the pipette, in order to 
thoroughly mix the fluids. Be careful lest the blood coagulate 
before the diluting fluid is drawn up, or an air bubble be drawn 
in through allowing the point of the pipette to slip out of the 
blood drops, and also lest by pressing the point of the pipette 
through the drop against the skin the column be prevented 
from rising. 



326 DISEASES OF THE BLOOD. 

The dilution of the blood is now 1 to 100. The counting- 
chamber, a disc of glass on which parallel lines are engraved 
to form 400 squares each -jo millimetre in length, is divided by 
double lines into groups of 16 squares. The depth when a 
cover glass is applied is yV of a millimetre. 

Blow out three or four drops from the pipette, and then de- 
posit a single small drop in the centre of the ruled disc and 



"$$&&&"& 



Fig. 24. — Blood-Counting Slide (Elevation). 

apply the cover glass accurately, so that no air bubbles are 
enclosed, and so that Newton's rings can be seen. 

Place the slide on the microscope in a horizontal position, 
and, using about a % inch objective, count the number of red 
corpuscles found in several of the groups of 16 squares each. 


























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Fig. 25. — The. appearance of the blood under the microscope, showing six- 
teen small squares enclosed by extra vertical and horizontal lines. 

In counting, include those corpuscles seen on the lower and left 
lines, but omit those seen on the upper and right lines. To 



DISEASES OF THE BLOOD. 327 

calculate, remember that each square has a cubic capacity of 

ioXiiX to = toW c.m.m. 

and therefore the formula for calculation must be 

No. of corpuscles counted X dilution (ioo) X 4ooo , 
number of squares counted ^ ~ = num ber of corpus- 

cles per c.m.m. of blood. 

In healthy men the red corpuscles are present to the number 
of about 5,000,000 per cubic millimetre, and in women about 
4,500,000 per c.m.m. In chlorosis the number is little changed, 
but in the other anemias it is often much diminished. 

(2) Counting the white corpuscles. This may be done with 
the special pipette, the diluting; solution being a Yi °/o solution 
of glacial acetic acid in water (to destroy the red corpuscles) 
with a small quantity of gentian violet added (to color the 
leucocytes). In this case the dilution is but 1 to 10; with this 
exception, the calculation is made from the count exactly as 
in the enumeration of the red blood corpuscles, viz. : 

No of corpuscles X dilution (10) X 4000 . . , 

« — r r 7—3 — number 01 leucocytes per 

Number of squares counted J F 

c.m.m. of blood. 

This method requires, on account of its larger pipette, such 
a quantity of blood that it is sometimes objectionable; and in 
consequence the ordinary pipette is often used for both counts. 

In health the number of white corpuscles varies from 5,000 
to 10,000 in every c.m.m. of blood. An increase of this 
number (leucocytosis, hyperleucocytosis) occurs physiologically 
during the digestion of proteids, and pathologically in many 
infectious and other diseases. A decrease {hypolencocytosis) 
occurs in certain other diseases, notably typhoid, tuberculosis, 
and malaria. 

Leucocytosis {hyperleucocytosis*) . — The causes of leucoc}i:osis 
are many. It occurs physiologically in the new-born, in preg- 
nant women, and after the ingestion of food. It occurs patho- 
logically in all the infectious diseases except tuberculosis, 
typhoid, malaria, influenza, and leprosy. Streptococcic and 



328 



DISEASES OF THE BLOOD. 



staphylococcic infections occasion a moderate increase of the 
number of leucocytes (15,000-40,000). Malignant tumors, 
especially sarcomata, the other cachectic conditions, and loss 
of blood by hemorrhage may give rise to a leucocytosis, and it 
may also be induced by various poisons (pilocarpine, cam- 
phor), certain bacterial toxins (tuberculin), etc. Leucocyto- 
sis is a symptom, not a disease, and of itself occasions no 
symptoms. When it exceeds 50,000 the existence of leuco- 
cythemia may be suspected. 

Hypoleucocytosis (leucopenia). — Decrease of the number of 
leucocytes (below 6,000) occurs notably in tuberculosis when 




Fig. 26. — Von Fleischl's Hemometer. 



no secondary infection has occurred and in typhoid fever; in 
cases where these diseases are suspected its discovery may 
have a decided diagnostic importance. In pneumonia an in- 
crease of leucocytes is the rule, but in some cases there is a 



DISEASES OF THE BLOOD. 329 

decrease, and the latter constitutes an unfavorable prognostic 
sign. Hypoleucocytosis is also found in the chronic sympto- 
matic anemias, in cases of malnutrition, etc., but is without 
direct clinical significance. 

3. The Estimation of the Amount of Hemoglobin is usually made by 
Von Fleischl's method, using the latter's hemometer (Fig. 
26). The small capillary tube which accompanies the 
apparatus, held by the stem (g) in which it is fixed, should be 
brought in contact with an exuding drop of blood, when it 
immediately fills by capillarity. Quickly clear the outside of 
any adherent blood and place it in the water of one compart- 
ment of the cylinder (d) y moving it about to dissolve out the 
coloring matter. Then, holding it vertically, allow drops of 
water from the pipette (//) to wash it clean, mix the blood and 
water thoroughly with the handle of the tube (g), and finally 
add water until the compartment is quite full. The other side, 
filled with water only, is placed over the wedge of colored 
glass (&). Artificial light, and as little of that as possible, is 
reflected upward through the cylinder, and the colored glass 
is moved backwards and forwards by jerks, until the tints of 
the two compartments appear to be about the same; then the 
percentage is read on the scale (z). 

Tallqvist's Method. — This simple method for estimating the 
amount of hemoglobin requires only a Tallqvist hemoglobin 
book, which contains specially prepared porous paper to soak 
up the blood, and a color table. The latter consists of ten 
color plates, the upper one representing the color obtained by 
soaking the porous paper in blood containing but 10% of 
hemoglobin, the next plate a facsimile of the color obtained 
by the use of blood containing 20%, and each succeeding plate 
representing the color effect of a blood 10% richer, up to the 
normal 100%. To perform the test, secure a drop or two of 
blood on the porous paper, allow it to dry until its gloss disap- 
pears, and then compare it with the color table. That plate 
to which the shade of color corresponds indicates the percent- 
age of hemoglobin. 

In chlorosis the amount of hemoglobin is greatly diminished, 



330 DISEASES OF THE BLOOD. 

without notable change in the number of red corpuscles. In 
the other anemias the amount of hemoglobin is decreased in 
proportion to the diminution in number of the red cells. 



SYMPTOMATIC ANEMIA. 

- Etiology.— Anemia may be secondary to: 

1. Hemorrhage. — Loss of blood, either from traumatism or 
in the course of a disease, produces an anemia which is severe 
in proportion to the amount and rapidity of the blood loss. 

2. Environment, Food, etc. — Insanitary surroundings and an 
unwholesome diet, by depressing the general health, have a 
marked effect upon the nutrition of the blood. 

3. Parasites. — The malarial parasite, certain gastrointes- 
tinal parasites, and the filaria sanguinis hominis are capable of 
inducing anemia by their interference with nutrition. 

4. Infections Diseases. — Anemia may be symptomatic of 
either an acute or a chronic infective process. 

5. Intoxications. — Toxins produced by gastro-intestinal dis- 
orders, or poisons from without (lead, mercury, etc.) may in- 
duce blood destruction. 

6. Organic Diseases and Neoplasms. — Diseases of the stom- 
ach, kidneys, lungs, and heart, and malignant tumors, may 
occasion anemia. 

Pathology. — In such a case examination of the blood reveals: 

1. Reduction of the amount of hemoglobin (from 75 to as 
low as 15%). 

2. Red corpuscles of irregular form, sometimes microcytes 
and megalocytes, and if the anemia is severe, nucleated red 
corpuscles. 

3. The proportion of leucocytes is often unchanged; some- 
times they are increased in numbers, and rarely they are de- 
creased. 

4. Chemical changes. The proportion of albumen is de- 
creased and that of water is increased. 



DISEASES OF THE BLOOD. 331 

Symptoms. — Among the symptoms suggestive of secondary 
anemia are: 

1. Pallor of the skin and mucous membranes. This may be 
slight, or it may amount to a deathly whiteness; in some cases 
the skin is yellow or gray in color. 

2. Emaciation. This is usually moderate in degree, and 
depends largely on the character of underlying conditions. 

3. The skin is frequently dry and harsh. 

4. G astro-intestinal disorders. Poor appetite, digestive dis- 
turbances, constipation, etc., usually accompany the anemia. 

5. Circulatory disorders. A rapid, weak heart, anemic 
murmurs, palpitation, dropsy, and serous effusions are com- 
mon in anemic states. 

6. Physical weakness and languor. 

7. Neuralgias. These may, however, be due to the under- 
lying cause. 

8. Dyspnea. Occasionally this is accompanied by dry cough. 

9. Menstrual disorders. Dysmenorrhea, amenorrhea, and 
rarely menorrhagia may occur. 

Diagnosis. — It is necessary to distinguish a symptomatic 
anemia from chlorotic anemia, in which there is a lack of the 
causal conditions enumerated. It occurs particularly in 
young girls, and is accompanied by a loss in hemoglobin 
entirely out of proportion to the decrease in number of the red 
corpuscles. 

Pernicious anemia is characterized by the presence of cer- 
tain varieties of corpuscles (microcytes, macrocytes, poiki- 
locytes, nucleated erythrocytes). 

Prognosis. — This varies according to the underlying cause 
and the possibility of its removal. 

Treatment. — 1. Discover and treat the underlying affection. 

2. Secure proper surroundings, sufficient hours of rest, and 
appetizing food. 

3. Administer such remedies as arsenicum, cinchona, iron, 
etc. 



332 DISEASES OF THE BLOOD. 

4. A severe post-hemorrhagic anemia may sometimes re- 
quire the use of saline infusions. 



CHLOROSIS. 

Etiology. — This is a primary anemia, occurring in young 
girls at puberty, to which heredity and improper surroundings 
seem to predispose. Older women and males are rarely 
affected. The exact cause is uncertain; it has been attributed 
to: 

1. Undeveloped heart and blood vessels, in some cases 
(Virchow). 

2. Infantile uterus and ovaries. 

Pathology. — 1, The blood is pale and abnormally fluid. 

2. The amount of hemoglobin is markedly reduced (60- 
20%). 

3. The red corpuscles are usually diminished but in lesser 
degree (4,000,000-1,500,000). 

Symptoms. — The patient, usually a young girl, presents: 

1. Pallor of the mucous membranes and skin, the latter 
often becoming greenish or yellowish in color. 

2. Digestive disorders (poor appetite, defective digestion, 
constipation, etc.). 

3. Circulatory symptoms (palpitation of the heart, some- 
times edema, and dyspnea, due to the deficiency of oxyhemo- 
globin). 

4. Menstrual disorders, especially amenorrhea. 

Physical Examination. — 1. Blood changes. There is no especial 
diminution in the number of erythrocytes, but a marked 
deficiency in the amount of hemoglobin. 

2. Anemic murmurs may be heard over the heart, and possi- 
bly dilatation of the latter may be detected. These murmurs 
are usually systolic in time, and are heard most frequently 
over the pulmonary area; but they may also present them- 
selves at the apex, over the tricuspid area, and at the aortic 



DISEASES OF THE BLOOD. 333 

orifice. A venous hum {bruit de diable) is heard over the root 
of the jugular vein. 

Prognosis. — The disease tends to spontaneous recovery in a 
few weeks, and prompt improvement under treatment is the 
rule. There is danger of relapse, however, and also of such 
serious complications as gastric ulcer and pulmonary tuber- 
culosis. Various cardiac, digestive, and nervous disorders 
may supervene. 

Diagnosis. — The age and sex of the patient, together with the 
marked disproportion in the decrease of hemoglobin as com- 
pared with that in the number of corpuscles, usually renders 
diagnosis easy. 

Treatment. — Personal hygiene. Rest, fresh air, and whole- 
some food are necessary. Avoid constipation. 

2. Medicines. Iron is the principal remedy; less often 
arsenic, manganese, strip Jiur, and other medicines are required. 

PERNICIOUS ANEMIA. 

Etiology. — This is a primary anemia of obscure origin. Gas- 
tric atrophy, intestinal parasites, and infective diseases have 
been credited with its production; and it may be secondary to 
oral sepsis, e. g., prolonged suppuration about a diseased 
tooth. 

Pathology. — Blood destruction is progressive, with a diminish- 
ing number of erythrocytes (even down to 150,000) and some 
reduction of the hemoglobin, but not proportionately. The 
number of leucocytes remains approximately normal. The 
liver becomes enlarged, fatty, and pigmented with iron; the 
bone marrow undergoes cellular hyperplasia, and degenerative 
and hemorrhagic changes occur throughout the viscera. 

Symptoms. — Pernicious anemia is characterized by : 

1. Pallor of the skin, which assumes a lemon-yellow tint. 
There is no emaciation. 

2. General anemic symptoms. Weakness, digestive dis- 
turbances, dyspnea, palpitation, syncope, edema, and hemic 
murmurs may be present. 



334 DISEASES OF THE BLOOD. 

3. The urine is of low specific gravity, and dark with patho- 
logic urobilin. 

4. Febrile attacks develop occasionally during the course of 
the disease. 

5. Blood changes. The blood appears thin, pale, and 
watery, like "meat washings." On microscopical examina- 
tion there is found to be: 

{a) A reduction in the number of red corpuscles to 
2,000,000 or below. 

(£) Megalocytes, microcytes, poikilocytes, and nucleated 
red corpuscles are present. 

(<:) The amount of hemoglobin is not proportionately de- 
creased. 
(d) The leucocytes are approximately normal in number. 
Prognosis. — The outlook is generally unfavorable; an ap- 
parent recovery is often but temporary. 

Treatment. — Should any focus of suppuration be found about 
the teeth, secure oral antisepsis by the use of carbolic acid (1 
in 40) or, better, let a dental surgeon remove all diseased 
tissue. Administer easily assimilable food (beef juice, pep- 
tonized milk) freely, and prescribe arsenic or such other 
remedies as may be symptomatically indicated. Febrile par- 
oxysms may suggest the advisability of using antistreptococcic 
serum. 

LEUCOCYTHEMIA. 

(Leukemia.) 

Etiology. — This is probably a disease of the blood-forming 
organs. Its exact cause, however, is unknown. It may be an 
infection. 

Pathology.— 1. The spleen becomes enlarged and adherent to 
adjacent structures. 

2. Lymphatic enlargements occur; the mesenteric, cervical, 
inguinal, axillary and other glands may become increased in 
size. 



DISEASES OF THE BLOOD. 335 

3. The bone-marrow becomes "pus-like," owing to the in- 
creased number of leucocytes. 

4. The liver, kidneys, and other organs undergo degenera- 
tive changes, and whitish nodules (consisting of proliferated 
leucocytes) may be found in them. 

Symptoms. — The patient presents — 

1. General anemic symptoms (pallor, gastrointestinal dis- 
turbances, dyspnea, etc.). 

2. Subjective discomfort due to the tumor (enlarged spleen) 
in left side of abdomen. 

3. Hemorrhages from the mucous membranes (nose, intes- 
tines, lungs, kidneys), or retina. 

4. Fever of irregular type with long intermissions. 

5. Lymphatic enlargements, the glands being soft and mov- 
able and producing no symptoms except by pressure upon 
adjacent organs. 

6. Blood changes. The blood may be simply pale, or it may 
even appear like pus, owing to the large number of leucocytes 
present. Microscopically it shows: 

(a) An enormous increase in the number of leucocytes (up 
to 600,000) so that in proportion to the red cells they are as 1 
to 50, 1 to 25, or even 1 to 2 or 3. The increase may be in the 
number of lymphocytes {lymphatic leukemia or lymphemia), 
but more commonly it is the myelocytes and eosinophiles 
{spleno-mednllary leukemia) which are increased. 

(b) The red corpuscles are somewhat diminished in number. 

(c) The proportion of hemoglobin is reduced. 

(d) Charcot's octahedral crystals appear in the blood if it is 
allowed to stand for a time. 

Diagnosis. — This is rendered possible by the blood examina- 
tion alone. An excessive leucocytosis is marked by an increase 
of the polynuclear neutrophiles only. 

Course and Prognosis. — The lymphatic form may be acute, 
proving fatal within two months. Other cases, while less 
rapid, usually terminate in death within two years. 



336 DISEASES OF THE BLOOD. 

Treatment. — Attend to the patient's hygiene and nutrition, 
and administer such remedies as arsenic, phosphorus, picric 
acid, and thuja. Inhalations of oxygen have been recom- 
mended, and extracts of bone marrow may be tried. Various 
symptoms, such as those due to digestive disturbances, con- 
stipation, and diarrhea, will present indications for special 
remedies. 



SPLENIC ANEMIA. 

Etiology. — The cause is unknown. 

Pathology. — Splenic anemia is distinguished by: 

1. Great enlargement of the spleen. 

2. Absence of enlargement of lymphatic glands. 

3. Absence of leucocytosis. 

Symptoms. — The course of splenic anemia is attended by: 

1. Enlargement of the spleen and attacks of severe pain in 
the splenic region. 

2. Fever of hectic type, reaching 102° or more in the even- 
ing. 

3. General anemic symptoms (weakness, digestive disturb- 
ances, palpitation, dyspnea, etc.). 

4. Hemorrhages from the mucous membranes. 

5. Blood changes of chlorotic type, i. e., the red corpuscles 
are reduced in number, with an even more marked diminuti- 
tion in the amount of hemoglobin. 

Diagnosis.— Leucocythemia is distinguished by a remarkable 
increase in the number of leucocytes. Pernicious anemia 
presents characteristic blood changes without splenic enlarge- 
ment. In Hodgkin s disease the anemia is not so profound, 
while the lymphatic glands are involved. Malignant disease 
of the spleen is marked by progressive emaciation and second- 
ary growths elsewhere, without pyrexia. SypJiilitic disease of 
the spleen may be distinguished by its history, associations, 
and by the therapeutic test. 



DISEASES OF THE BLOOD. 337 

Prognosis. — Hopeless; death from asthenia occurs within two 
years. 

Treatment. — This must of necessity be symptomatic. 

HODGKIN'S DISEASE. 

(Pseudo-Leukemia; Lymphatic Anemia; Lympho-Sarcoma. ) 

Etiology. — The exciting cause is unknown. 

Pathology. — Pseudo-leukemia presents the following lesions: 

1. Hyperplasia of the lymph glands: The cervical lym- 
phatics are the first to become enlarged, and the axillary and 
inguinal glands are next affected. Suppuration in these en- 
larged glands is a rare occurrence. 

2. Hypertrophy of the spleen occurs in 80 per cent, of the 
cases. 

3. New formations of lymphatic tissue may appear in any 
tissue of the body, especially in the liver, kidneys, lungs, and 
heart. 

Symptoms. — Hodgkin's disease is characterized by: 

1. General anemic symptoms. (Languor, dyspnea, palpi- 
tation, digestive weakness, etc.). 

2. Enlargement of the lymphatic glands, usually detected 
first in the neck. Later, when they have increased in size, 
they project as large bunches. Subsequently similar enlarge- 
ments are found in the axilla and groin. 

3. Enlargement of the spleen. This gives rise to a sensation 
of heaviness or dragging, or even actual pain. The enlarged 
organ may be grasped through the abdominal walls. 

4. Febrile paroxysms of irregular type. These often coin- 
cide with the involvement of new groups of glands. 

5. Blood changes. At first the blood is practically normal, 
but later there is an anemia of symptomatic type. 

Diagnosis. — The diagnosis rests upon the discovery of the 
lymphatic enlargements, unassociated with any characteristic 
blood changes. Tuberculous glands are found in younger 
22 



338 DISEASES OF THE BLOOD. 

persons, are generally unilateral, and tend to suppurate, while 
the spleen and liver are not so markedly enlarged. Syphilitic 
enlargement of the glands may be distinguished by the history, 
the associated symptoms, and the therapeutic test. Leucocy- 
themia presents a striking increase in the number of leu- 
cocytes. 

Prognosis. — This is very unfavorable; death from exhaustion 
usually occurs within three years. 

Treatment. — The patient's surroundings should be made as 
hygienic as possible, and his food must be nutritious and 
easily digestible. Surgical removal of the glands should be 
considered early in the disease, in the hope of thus arresting 
its progress. The principal remedies are arsenic, arsenic 
iodide, iodine, iron, mercurius biniod., and phosphorus. 

ANEMIA INFANTUM PSEUDO-LETJKEMICA. 

Etiology. — This rare affection occurs in chilren under the age 
of four, and especially between the seventh and twelfth 
months of life. Rickets, hereditary syphilis, and gastro- 
intestinal disturbances seem to predispose to it. 

Pathology. — The spleen becomes increased in size, the liver 
and lymphatic glands are often enlarged, and the bone mar- 
row may be reddened and soft. 

Symptoms. — 1. The spleen is enlarged and may be distinctly 
felt projecting from beneath the ribs into the abdomen. It is 
extremely hard. 

2. Pallor, weakness, emaciation, and other evidences of 
anemia are present. 

3. Blood changes, (a) The red corpuscles are reduced in 
number below 3,000,000. Poikilocytes and erythrocytes are 
common. 

(b) Marked leucocytosis is present, and the polynuclear 
leucocytes may be increased to 100,000 or more. 

Diagnosis. — Leucocythemia may be excluded by discovery of 
the fact that the increase is in the number of polynuclear 



DISEASES OF THE BLOOD. 339 

leucocytes. The lack of hepatic enlargement and of glandular 
involvement, the co-existing evidences of rickets or hereditary 
syphilis, and the comparatively benign course also serve to 
distinguish the disease. 

Prognosis. — The anemia is progressive, but under proper 
treatment it tends to recovery. 

Treatment. — Pay close attention to the general hygiene of 
the patient, see that the child has a suitable nutritious diet, 
and prescribe such remedies as arsenic, iodide of arsenic, 
iodide of iron, and pliosphorits. 

HEMOPHILIA. 

(Hemorrhagic diathesis; Bleeder's disease.) 

Etiology. — Heredity appears to be the only important predis- 
posing cause of hemophilia. 

Pathology. — It is undecided whether the bleeding is due to 
chemical changes in the blood or to changes in the vessel 
walls. 

Symptoms. — In a "bleeder," profuse and persistent hemor- 
rhage follows trivial injury or even occurs spontaneously. It 
usually is limited to a capillary oozing, which may occur from 
or beneath the skin or mucous membranes or into the joints, 
and is often uncontrollable. 

Diagnosis. — The tendency to uncontrollable hemorrhages 
usually appears in childhood, and inquiry often reveals the 
family predisposition. 

Prognosis. — In many cases hemorrhage proves fatal in early 
life. If the child survives this danger, the tendency may be 
outgrown. 

Treatment. — The treatment should be largely prophylactic; 
the child ought to be guarded against the slightest traumatism. 
He should be carefully nourished, and at the same time hard- 
ened by a judicious out of door life. Attacks of hemorrhage 
must be met by surgical measures, the subsequent treatment 
being that of secondary anemia. 



340 DISEASES OF THE BLOOD. 



PURPURA. 

Purpura is a generic term used to designate a number of 
conditions characterized b} 7 hemorrhages into the skin. 
Varieties. — 1. Primary purpura includes: 

(a) Simple purpura; this is a form characterized by pete- 
chial or ecchymotic extravasations into the skin, the cause of 
which is unknown. 

(b) Arthritic purpura (Purpura rheurnatica, Peliosis rheu- 
matica, Sckdnleiri s disease} is a form characterized by swollen 
and painful joints, a purpuric eruption, and edema of the feet 
and ankles. It is accompanied by mild fever (101° to 103°). 
Severe gastro-intestinal disturbance may be associated 
(Henoch 's purpura). The prognosis is favorable provided no 
complications (endocarditis, intestinal hemorrhage, hemor- 
rhagic nephritis) arise. 

(c) Hemorrhagic purpura (Morbus Weilhofii) is a form 
characterized by extensive subcutaneous ecchymoses and 
hemorrhages from the mucous membranes of the respiratory 
and gastro-intestinal tracts, or into the brain, kidneys, or 
serous cavities. It is accompanied by fever and prostration, 
and is often fatal. 

2. Secondary purpura may be symptomatic of: 

(a) Infectious diseases, including cerebro-spinal fever, 
variola, septicemia, pneumonia, and the exanthemata. 

(b) Profound blood changes such as occur in leukemia, 
scurvy, and the various cachexias. 

(c) Degenerations of the arterial walls, such as occur in 
arterio-sclerosis, sometimes as the result of syphilis, nephritis, 
etc. 

(d) The ingestion of toxic substances, such as quinine 
belladonna, ergot, mercury, the iodides, and the snake 
poisons. 

(e) Mechanical strains, such as violent coughing and con- 
vulsions. 



DISEASES OF THE BLOOD. 341 

(/) Neurotic conditions, e. g., vaso-motor relaxation due to 
hysteria, spinal cord inflammation, etc. 

(g) Hemophilia. 

Treatment of Purpuric Diseases. — In the secondary purpuras, 
treatment should be directed to the causal condition. In 
simple purpura, arsenic is of great value. In rheumatic pur- 
pura the most important remedies are bryonia, arnica, ledum, 
mercurius, and belladonna ; and in hemorrhagic purpura ar- 
senic, lachesis, naja, or phosphorus is usually indicated. 

SCURVY. 

(Scorbutus.) 

Etiology. — This disease is the result of depraved vitality, 
due to: 

1. Improper diet, i. e., an insufficient supply of fresh vege- 
tables. 

2. Insanitary surroundings. 

3. Infection. Analogy affords ground for a suspicion that 
the disease may be infectious. 

Pathology. — 1. Profound anemia of symptomatic type, with 
fatty degeneration of the viscera. 

2. Hemorrhagic effusions into all tissues and into the joints. 
Symptoms. — The disease is gradual in its onset, presenting: 

1. General anemic symptoms, including pallor, emaciation, 
weakness, palpitation, and edema. Irregular fever may occur, 
and gastro-intestinal disturbances, especially diarrhea, may 
be prominent. 

2. Hemorrhagic symptoms. The gums become swollen and 
tender and bleed readily. The teeth may be loosened or even 
drop out. Ecchymotic spots appear on the skin, especially 
about the ankles, and occasionally ulceration follows. Sub- 
periosteal hemorrhages are common, especially in children, 
and may lead to pain and swelling in the affected limbs. 
Bleeding may arise from any of the mucous membranes, 
and constitutes a serious symptom. 



342 DISEASES OF THE BLOOD. 

Prognosis and Clinical Course. — Under suitable conditions the 
prognosis is favorable. The course of the disease is chronic, 
extending over weeks, and death may finally occur from as- 
thenia, edema of the lungs, pneumonia, or diarrhea. Anky- 
losis may follow hemorrhage into a joint. 

Treatment. — Fresh air, fresh vegetables and fruit juices suffice 
to cure the disease. Convalescence may be hastened by the 
use of mercurius or the mineral acids (hydrochloric, nitric, or 
sulphuric). Hemorrhagic symptoms require arsenic, cinchona, 
crotalus y hamamelis, lachesis, phosphorus, or terebinth. 

INFANTILE SCURVY. 

(Barlow's Disease.) 

As the result of the exclusive use of condensed milk or other 
preserved foods, infants are prone to develop subperiosteal ex- 
travasations of blood, which cause thickening and tenderness 
in the shafts of the long bones. There may also be inter- 
muscular hemorrhages, but as a rule the joints escape. The 
child becomes anemic and feverish, and the pain on motion 
causes it to lie motionless, with the legs drawn up, and to cry 
out when moved. Prompt recovery follows the administra- 
tion of fresh milk, beef juice, and the juices of orange, lemon, 
pine apple, etc. The remedies mentioned above include those 
ordinarily required by children. 



DISEASES OF THE DUCTLESS 
GLANDS. 



ADDISON'S DISEASE. 

Etiology. — The lesions of the adrenal bodies, as the result of 
which the physiological activity of these glands may be 
abolished, are as follows: 

1. Tuberculosis, with fibro-caseous degeneration or calcifi- 
cation. 

2. Degeneration, fatty or cystic. 

3. Atrophy, simple or following chronic interstitial inflam- 
mation. 

4. Malignant disease (carcinoma or sarcoma). 

5. Hemorrhagic extravasation or embolism. 

It is probable that these glands furnish an internal secretion 
essential to normal metabolism, failure of which is followed 
by the group of symptoms known as Addison's disease. An- 
other theory, however, ascribes the disease to the abdominal 
sympathetic system and regards the pigmentation as a trophic 
phenomenon. 

Symptoms. — 1. Pigmentation of the skin (melasma), the 
color varying from a light yellow to brown or almost black. 
This bronzing is deeper on exposed portions of the body, often 
appears on the mucous membranes, and may be associated 
with whitish patches of leucoderma. The tint is never uni- 
form all over the body, even in extreme cases. The patches 
shade off gradually and have no abrupt margins. 

2. AstJienia. The patient suffers with languor and debility, 
the heart's action is feeble, the pulse is small in volume and 
low in tension, and a symptomatic anemia is present. Ema- 
ciation does not occur. 



344 DISEASES OF THE DUCTLESS GLANDS. 

3. Gastric irritability. The patient suffers more or less 
with anorexia, nausea, and vomiting. 

Diagnosis. — Pigmentation of the skin is not pathognomonic 
of Addison's disease; it is sometimes associated with tubercu- 
losis of the peritoneum, abdominal neoplasms, pregnancy, and 
uterine and hepatic diseases, and the possibility of each of 
these should be excluded. Jaundice, unlike Addison's disease, 
colors the conjunctiva and the urine. Argyria, the pigmen- 
tation resulting from the long-continued ingestion of silver 
nitrate, can be distinguished by the history. The co-existing 
asthenia and gastric irritability are strong confirmatory signs 
of Addison's disease. It has been suggested that, since a 
majority of the cases are tubercular, the tuberculin test be 
applied to doubtful cases. 

Prognosis. — The disease is invariably fatal. The duration 
varies from a few months to several years, death occurring, as 
a rule, from asthenia. 

Treatment. — Conserve the patient's strength by keeping him 
at rest. The food should be easily assimilable and highly 
nourishing, and stimulants frequently become necessary. 
Nausea may be relieved by carbonated waters, koumiss, cham- 
pagne, etc. Arsenic and argentum nit. are strikingly indi- 
cated in many cases and unquestionably serve to control the 
symptoms for which they are prescribed. Calcarea ars., 
iodine, and theridio?i have also been recommended, and the 
administration of suprarenal extract, gr. iij-vi, t. i. d., may 
be tried. 



GOITRE. 

(Bronchocele; Derbyshire Neck; Struma.) 

Etiology. — The exciting cause of this enlargement of the 
thyroid gland is unknown. Certain drinking waters, or rather 
some constituent of them, have been proven to produce goitre, 
and iron pyrites, copper pyrites, sulphate or carbonate of lime, 
and carbonate of magnesia are among the substances credited 



DISEASES OF THE DUCTLESS GLANDS. 345 

with this action. In certain localities in Europe goitre is 
endemic, but in this country it is only sporadic. 

Pathology. — According to their anatomical features, goitres 
are divided into the parenchymatous, a simple hypertrophy of 
the gland; the fibrous, in which the increase is chiefly of con- 
nective tissue; the cystic, in which the normal follicles become 
enlarged to form cysts with liquid contents; the colloid, in 
which the cysts contain a colloid material; the calcareous, in 
which calcareous infiltration occurs ; and the amyloid, in which 
there is a wax-like product. Rarely the enlargement is asso- 
ciated with great dilatation of the vessels, whereby a forcible 
expansile pulsation is imparted to the gland — pulsating goitre. 

Symptoms. — Subjective symptoms are usually lacking, the 
only characteristic indication of the disease being a swelling 
over the region of the thyroid which moves with the larynx in 
deglutition. By pressure the enlarged gland may cause 
dyspnea or dysphagia, or by interference with nerves, espe- 
cially the pneumogastric, it may induce spasm of the glottis or 
paralysis of one or both vocal cords. 

Treatment. — Iodine, used locally and internally, is the leading 
remedy. Baryta iod., bromine, calcarea carb., kaliiod., Phyto- 
lacca, and spongia are also recommended. In obstinate cases 
an alcoholic solution of iodine may be injected, electrolysis 
may be attempted, or surgical extirpation of the gland may be 
resorted to. Patients should either remove from a goitrous 
district or drink only boiled water. 

EXOPHTHALMIC GOITRE. 

(Grave's or Basedow's Disease; Tachycardia Vasomotoria.) 

Etiology. — Two theories as to the origin of exophthalmic 
goitre are in vogue, viz. : 

1. That it is due to a lesion in the medulla or the sympa- 
thetic nervous system. 

2. That it is the antithesis of myxedema, being due to over- 
activity of the thyroid gland. 



346 DISEASES OF THE DUCTLESS GLANDS. 

Symptoms. — Four symptoms are conspicuous features of this 
disease, though one or more of them may be absent in a given 
case. 

1. Tachycardia. The pulse rate is usually above 100, and 
may reach 200. The heart impulse is strong, the sounds are 
loud, and a soft blowing murmur is often heard at the base. 

2. Exophthalmos. Both eyeballs may be protuberant, 
though sometimes one is more so than the other; and at 
times the protrusion is so great that the lids are unable to 
close. In some cases the lid does not not follow the eye when 
it is cast downward or raised (von Graefe's sign), or there may 
be increased width of the palpebral fissure, owing to the retrac- 
tion of the upper lid (Stellwag's sign). The patient winks 
less frequently than is normal. 

3. Thyroid enlargement can usually be discovered; it is mod- 
erate in degree, by no means as great as in a case of simple 
goitre. Pulsation and thrill may be detected on palpation, 
and auscultation reveals a blowing murmur. 

4. Tremor is almost invariably present. It is very fine, be- 
comes aggravated under any excitement, and is associated 
with vague "general nervousness." 

Various other symptoms, such as menstrual disturbances, 
local or general edema, gastro-intestinal derangement, etc., 
may be noted in connection with some cases. 

Diagnosis. — In the presence of tachycardia search should 
always be made for other evidences of exophthalmic goitre. 
The discovery of slight temporary enlargement of the thyroid 
or of tremor will justify a positive diagnosis. Without the 
presence of tachycardia, however, no case can be considered 
one of exophthalmic goitre. 

Prognosis.— The disease is chronic in its course, usually per- 
sisting for several years. Under proper treatment a majority 
of the patients improve and many recover. Death may occur 
from heart failure or intercurrent disease. 

Treatment. — Rest, preferably absolute for a time, and freedom 
from excitement, are essential preliminaries to successful treat- 



DISEASES OF THE DUCTLESS GLANDS. 347 

ment. The diet should be highly nutritious, and daily massage 
and a morning cold sponge bath are advantageous. Lycopus 
is usually the most efficient medicine, but indications may 
exist for the administration of arsenic, aurum, belladonna, 
ferrum, glonoin, iodine, sulphur, and many other drugs. 



MYXEDEMA. 

Etiology. — As a result of some change in the thyroid gland 
which renders the latter functionless, a substance essential to 
general nutrition, probably a secretion, is no longer elaborated; 
and in consequence a solid edematous swelling of the sub- 
cutaneous tissues appears. 

Symptoms. — The disease is much more common in women 
than men, and is apt to appear during middle life. The onset 
is insidious, the condition becoming noticeable only when the 
nutritional change is so advanced that the patient's face is 
uniformly swollen and flattened, the nose being broad, the 
eyelids puffed, and the usual wrinkles obliterated. The skin 
is dry and harsh, pale and waxy in appearance, and does not 
pit on pressure. The hands are swollen and "spade-like," 
and the feet are enlarged. The mind is torpid, mental pro- 
cesses are slow, and dementia may ensue. The temperature 
is subnormal. 

Cretinism is myxedema occurring in infancy or childhood, 
as the result of which there is an almost complete arrest of 
mental and physical development, and the patient becomes an 
idiot and a dwarf. The general symptoms do not differ from 
those of adult myxedema. 

Operative myxedema {cachexia strtimipriva) is myxedema 
following surgical extirpation of the thyroid gland. 

Diagnosis. — The swollen appearance, with the absence of 
pitting on pressure, the harsh, dry skin, the slowness of 
thought, speech, and action, and the subnormal temperature, 
form a clinical picture which is unmistakable. 

Prognosis. — Previous to the introduction of thyroid feeding 
the prognosis was hopeless, but under that method of treat- 



348 DISEASES OF THE DUCTLESS GLANDS. 

ment the symptoms of myxedema can be entirely removed in 
a few months. 

Treatment, — During the early stage of the treatment keep 
the patient at rest, and administer from 3 to 10 grains of the 
powdered extract, or from 15 to 30 minims of the glycerine 
extract of the thyroid gland, three times a day. Watch the 
effect carefully; acceleration of the pulse demands reduction 
in the dose, while a fall of temperature or a slight increase of 
the swelling requires an increase. As improvement begins 
the dose may be reduced slightly. After the myxedema has 
been removed a single small daily dose must be continued for 
an indefinite period. 



CONSTITUTIONAL DISEASES. 



DIABETES MELLITUS. 

Etiology. — Among the causes predisposing to diabetes mel- 
litus are heredity, male sex, and middle life. Intellectual 
workers, the better classes, and especially Hebrews, are 
among those most often affected. The obese are liable to the 
alimentary form, while a special variety is due to traumatism, 
especially injuries to the head. 

Pathology. — Diabetes is in reality a generic term, for glyco- 
suria may result from: 

1. Organic disease of the pancreas. Extirpation of the 
pancreas is followed by glycosuria, and that organ is found 
diseased in a majority of diabetics; and these include the most 
severe cases. 

2. Interference with the glycogenic function of the liver. 
This may result from disease of that organ or of the nervous 
system (puncture of the floor of the fourth ventricle, section 
of the pneumogastric nerve, etc.). These are the cases which 
follow central or spinal disease. 

3. Ingestion of an excess of carbohydrates. If more carbo- 
brydrates are taken into the body than can be consumed in the 
tissues or stored in the liver as glycogen, the excess finds its 
way into the urine as sugar. This constitutes alimentary 
glycosuria. 

Morbid Anatomy. — The post mortem findings are not distinct- 
ive. The most common is a granular atrophy or other de- 
generative change in the pancreas; rarely, organic disease 
(tumors, sclerosis, etc.) is found in the medulla, and yet more 
rarely there is primary disease of the liver. The proportion 
of sugar in the blood is increased, and the profound influence 



350 CONSTITUTIONAL DISEASES. 

of the disease on general nutrition is demonstrated by second- 
ary changes in many organs, including the liver, kidneys, 
heart, lungs, brain, cord, and peripheral nerves. Peripheral 
neuritis is particularly common, and when multiple has been 
incorrectly termed diabetic tabes. 

Symptoms. — An immense number of symptoms, none of them 
necessarily distinctive, may be grouped about the essential 
ones of glycosuria, polyuria, thirst, and wasting. They may 
be classed as: 

1. General Symptoms. — Bodily and intellectual weakness 
comes on gradually, with increasing emaciation, distressing 
thirst, and insatiable hunger. 

2. Cutaneous Symptoms. — The skin becomes dry and harsh, 
itching is often intolerable, the hair may fall out, and boils 
and carbuncles are common. Gangrene may supervene. 

3. Nervous Symptoms. — Depression of spirits, headache, 
and an irritable temper are common in diabetics. Peripheral 
neuritis may occasion localized numbness, tingling, trophic dis- 
turbances, and loss of reflexes {diabetic tabes). Diabetic 
coma may furnish a terminal catastrophe. 

4. Urinary Phenomena. — The urine is increased in quantity, 
and this increase is sometimes so great that it is remarked by 
the patient and brings him to the physician. It is pale in 
color, acid in reaction, its specific gravity is high (1020-1065), 
and it contains sugar in amounts varying from Yz to 10 per 
cent. Albumin is not unusual. 

Clinical Varieties. — By the severity of the clinical manifesta- 
tions two distinct forms of the disease may be recognized, 
which also presumably differ in their underlying cause, viz. : 

1. Pancreatic Diabetes. — This is a severe varietv in which 
dietetic restriction is unavailing, albuminoid disintegration 
being persistent, the patient becoming extremely emaciated 
and dying within a few years. 

2. Alimentary (Lipogenic) Glycosuria. — This is a mild 
variety due to excessive eating and drinking and physical in- 
activity. It occurs, therefore, in the obese, in those beyond 



CONSTITUTIONAL DISEASES. 351 

middle life, and is frequently associated with gout. As a rule 
it can be controlled by proper dietetic restrictions. 

Course. — Some cases of diabetes, especially in the young, are 
acute in onset and run a rapidly fatal course. They are prob- 
ably of pancreatic origin. A majority of even the severe cases 
run a more or less protracted course extending over several 
years, death finally occurring from one of the complications 
or from coma. The alimentary form is compatible with a long 
life, the tendency being to the supervention of nephritis. 

Complications. — Gangrene, tuberculosis, arterio-sclerosis, car- 
diac weakness, interstitial nephritis, cataract, optic neuritis. 

Diagnosis. — By the discovery of persistent glycosuria. 

Prognosis. — An onset late in life, in association with obesity 
or gout, slight glycosuria, tolerance for a certain quantity of 
carbohydrates, and circumstances which permit hygienic and 
dietetic restrictions render the prognosis for life quite favor- 
able. On the other hand, youth, rapid loss of strength, grave 
complications, intense glycosuria, intolerance of even small 
amounts of carbohydrate food, and poverty, render the pros- 
pect unfavorable. In any case, imminence of coma and a 
fatal issue is indicated by the appearance of diacetic acid in 
the urine. (For test, see page 201.) 

Treatment. — 1. Dietetic. At once place the patient on a diet 
free from carbohydrates; it may include meats, soups, oysters, 
clams, fish, poultry, game, eggs, green vegetables, spinach, 
celery, salads, butter, cheese, tea, coffee, whisky, and mineral 
waters, These articles must be prepared without sugar or 
dressings which contain flour. Saccharine may be used to 
sweeten the tea or coffee. Following the adoption of this 
diet, examine the urine daily for a week. By the end of that 
time sugar will have disappeared in mild cases and will be 
much diminished in those of moderate severity. Then allow 
the patient a definite, weighed quantity of carbohydrates 
(wheaten bread or baked potato) daily. If the first quantity, 
say 4 ounces, does not cause a reappearance of the sugar, or 
an increase over the previous minimum, cautiously increase 



352 CONSTITUTIONAL ^DISEASES. 

the amount of carbohydrate until the glycosuria does reappear 
or increase. Then drop back to the largest amount of carbo- 
hydrate food which was tolerated without increase of sugar, 
which may be considered the patient's maximum allowance. 

2. Hygienic. The patient must live in the open air as much 
as possible, must exercise moderately but persistently, and he 
should take a cool sponge bath on arising in the morning, and 
a tepid bath at least twice a week on retiring. 

3. Medicinal. Indications may be found for many reme- 
dies. Uranium nitrate is particularly indicated in severe, 
presumably pancreatic, cases, and its effects are sometimes 
striking. Phosphoric acid is advisable for over-worked, weak, 
neurotic patients who pass large quantities of highly saccharine 
urine, rich in phosphates or oxalates. PJiosphorus may be 
preferred for older persons with degenerated tissues. Arsenic 
or sodium arsenite is useful in cases where anemia, gastro- 
intestinal disturbances, and cutaneous symptoms are promi- 
nent. Aurum is suggested by cardiac weakness associated 
with neurotic symptoms. A complicating nephritis may call 
for the administration of aurum, plumbum, or plumbum iodide. 
Special symptoms will afford indications for other remedies. 



DIABETES INSIPIDUS. 

Etiology. — This disease is marked by prolonged excretion of 
an excessive quantity of non-saccharine and non-albuminous 
urine. Its cause is unknown, but a large proportion of cases 
is associated with cerebral disease or injury, and inasmuch as 
puncture of the floor of the fourth ventricle above the diabetic 
centre produces polyuria, it seems probable that the lesion 
lies in the nervous system. 

Symptoms. — The principal symptom is increased secretion of 
urine, the quantity varying from six to forty pints in twenty- 
four hours. The urine is pale, often clear as spring water, and 
of low specific gravity. In addition the patient complains of 
intense thirst, and there is dryness of the skin and absence of 



CONSTITUTIONAL DISEASES. 353 

perspiration. The appetite is voracious, but the patient be- 
comes progressively feeble and emaciated, and complains of 
vague nervous symptoms. The course of the disease varies 
greatly; the patient may die from exhaustion within twelve 
months, or he may live for years and finally die of some inter- 
current affection. 

Diagnosis. — Simple polyuria, the result of nervous conditions, 
diuresis, or excessive imbibition of fluids, is readily distin- 
guished by its temporary character. 

Interstitial nephritis may for a time present a large amount 
of non-albuminous urine, but persistent re-examination will 
finally reveal albumin and tube casts, which, in association 
with cardio-vascular changes, permit of no diagnostic doubt. 

Prognosis. — Recovery is not infrequent, and death occurs, as 
a rule, only in cases with symptoms indicating a serious nerve 
lesion. Many cases are protracted but "troublesome rather 
than dangerous." 

Treatment. — No limitation of the amount of fluids consumed 
is advisable. Medicines should be prescribed in accordance 
with the S3 r mptomatic indications, the more important being 
argentum, aurum, murex, phorphoric acid, scilla, strophan- 
thus, uranium, and valerian. 

GOUT. 

Etiology. — An abnormal accumulation of uric acid in the 
blood and tissues may be the result of: 

1. Heredity (60%). 

2. Excessive indulgence in rich food and liquors. 

3. An inactive life. 

The disease occurs more frequently in males and in middle 
or advanced life. Lead-poisoning is a contributing cause in 
some cases. 

Pathology. — As the result of decreased elimination or in- 
creased formation an excess of uric acid is found in the blood, 
and in the form of sodium urate it may be deposited around 
23 



354 CONSTITUTIONAL DISEASES. 

the fibrous structures of the small joints, especially the great 
toe. The deposit may be uniform throughout the tissue, or it 
may appear in small opaque areas, forming "chalk stones" 
(tophi). The latter appear upon the digital joints, the carti- 
lages of the ear, and less often about the vocal cords, the 
cartilages of the nose, etc. Those about the joints sometimes 
ulcerate through the skin. Ultimately sclerotic changes are 
induced in the arterial system, the kidneys, and other organs. 

Varieties. — 1. Regular gout (acute or chronic). 

2. Irregular gout (lithemia; uric acid diathesis). 

Symptoms. — Acute gout. Often after symptoms of indiges- 
tion or some similar disorder the patient is seized with agoniz- 
ing pain in one of his joints, usually the metatarso-phalangeal 
joint of the great toe, about which there is swelling, heat, and 
discoloration of the skin. There is moderate fever (100- 
102°), and the urine is scanty, dark-colored, of high specific 
gravity, and contains an excess of uric acid and urates. In the 
course of some days the symptoms subside gradually, the 
joints become more supple, the skin over the affected articula- 
tion desquamates, and convalescence ensues. 

Gout is said to be retrocedent when it suddenly disappears 
from the joints and occasions derangement of some internal 
organ, such as the brain, heart, stomach, or bladder. Such 
cases may properly be regarded as forms of irregular gout, 
however. 

Chronic gout represents the gradual accumulation of morbid 
changes induced by repeated acute attacks. The joints be- 
come filled with chalky deposits, immobility and deformity 
ensue, and finally cardio-vascular degeneration and chronic 
interstitial nephritis become associated with the arthritic con- 
ditions. 

Irregular gout includes a variety of symptoms which are not 
in themselves distinctive, but which represent a condition of 
disturbed metabolism with an excess of uric acid in the blood. 
It lacks the uratic deposits in the tissues and the other 
localized manifestations of regular gout, and instead presents 



CONSTITUTIONAL DISEASES. 355 

-a wide variety of nervous symptoms (headaches, neuralgias, 
insomnia, lumbago, etc.), digestive disturbances (coated 
tongue, dyspeptic symptoms, gastralgia, hyperchlorhydria, 
and constipation), and various cutaneous irritations (pruritus, 
eczema, etc.), together with circulatory and respiratory dis- 
orders. In this, as in the regular form, the diagnosis rests upon 
the urinary phenomena. 

Diagnosis. — Regular gout may be mistaken for rheumatism, 
but the latter usually affects larger joints, such as the knee 
and elbow, presents higher fever and profuse acid sweats, and 
desquamation of the epidermis rarely follows the attack. 

Irregular gout may simulate various nervous and gastroin- 
testinal affections, and often is passed over as " malaria" or 
"rheumatism;" but the acid, high-colored, scanty urine, 
loaded with uric acid and urates, while not in itself absolutely 
diagnostic, becomes conclusive evidence when associated with 
the history and symptoms detailed. 

Prognosis. — In acute gout and in irregular gout, treatment is 
usually effective. In chronic gout, and when secondary 
changes have occurred in heart, arteries, and kidneys, the 
outlook is much less favorable. 

Treatment. — 1. Diet. Meats, alcohol, tea, coffee, and to- 
bacco must be restricted, while milk, butter, fruits, and succu- 
lent vegetables are recommended. A moderate amount of 
fish, oysters, and poultry may be substituted for butcher's 
meat. 

2. Hygiene. The patient should take a morning cold bath 
or an evening warm bath daily, the bowels and skin should be 
kept active, and he should exercise regularly in the open air. 

3. Medicines. During an acute attack the patient should 
remain in bed with the affected joints wrapped in cotton, and 
the administration of colchicum or colchicine is generally indi- 
cated. In some cases aconite, arnica, belladonna, benzoic acid, 
or the benzoates, berberis, or bryonia may be preferable. In 

the periods between attacks or in cases of irregular gout a 
great variety of remedies, especially berberis, lycopodium, 



356 CONSTITUTIONAL DISEASES. 

sepia, and sulphur, may be syrnptomatically indicated; but it 
must be remembered that cure depends almost entirely upon 
proper diet and habits of living. 



ARTHRITIS DEFORMANS. 

(Rheumatoid Arthritis; Rheumatic Gout; Osteoarthritis.) 

Etiology.— This deforming disease of the joints occurs inde- 
pendently of rheumatism or gout and their causes. It attacks 
women much more frequently than men, and the more im- 
portant predisposing causes .are heredity, traumatism, insuf- 
ficient food, and such neurotic factors as shock and worry. 

Pathology. — The exact nature of the process is undecided, 
many regarding it as of neurotrophic origin, and others con- 
sidering it but a manifestation of the arthritic diathesis. The 
joint changes consist of proliferation of the cartilage cells, 
followed by fibrillation of the intercellular substance and sub- 
sequent degeneration, liquefaction, and absorption, which 
leaves the bone ends bare; the latter finally become smooth 
and eburnated. The remaining peripheral margin of cartilage 
thickens and forms bony outgrowths {osteophytes), the syno- 
vial membrane becomes thickened and its fringes hyper- 
trophied, and as a result the joint is stiffened and creaks 
or grates when moved, the muscles about it undergo atrophy, 
and great deformity ensues. 

Symptoms. — The onset of the disease is very insidious. The 
patient, often a youngish woman, notices a little tenderness or 
swelling in a joint, and soon one or more articulations be- 
come painful, swollen, and inclined to creak on motion. 
Nodules develop on the sides and ends of the distal phalanges 
of the fingers and sometimes the toes (Heberden's nodosities, 
seen also in gout). The ligaments about the joints become 
thickened, and muscular contractures flex the limb in an ab- 
normal position. The disease advances slowly, often by a 
series of acute exacerbations which attack fresh articulations. 
There is a tendency to involve corresponding joints on the 



CONSTITUTIONAL DISEASES. 357 

two sides, the disease progressively invading the small joints 
of the hands, the knees, the feet, ankles, wrists, elbows, 
shoulders, hip joints, and even the spinal column. The joints 
become less and less mobile and undergo flexion and con- 
tracture, so that finally the fingers are bent backward and 
turned toward the ulnar side, the thighs are drawn up, the 
legs adducted and flexed, and the condition of the motionless 
and distorted patient is truly pitiable. She becomes emaci- 
ated and anemic, suffers much pain at times, and yet lives for 
years. 

Varieties. — Multiple arthritis deformans, in which the large 
joints are progressively invaded. 

A partial or monoplegic form, limited to one or two joints, 
which is particularly common in the hip-joint of elderly men 
and is associated with wasting of the muscles of the buttock 
and the thigh. 

Diagnosis. — Gout is distinguished by tophaceous deposits and 
an excess of uric acid in the blood and urine. Rheumatism is 
accompanied by a fever and a tendency to heart complica- 
tions. The arthropathies of locomotor ataxia and syringo- 
myelia are distinguished by the associated symptoms and the 
absence of osteophytes. 

Prognosis. — Generally unfavorable, though spontaneous ar- 
rest may occur. The duration is protracted, death occurring 
only as the result of intercurrent disease. 

Treatment. — Improve nutrition by the use of such foods as 
cream, butter, fat meat, and cod liver oil. Maintain joint 
movement by active and passive movements and massage. 
Steam or electric baths and local galvanism may be tried. Of 
medicines, calcarea, cimicifuga, Pulsatilla, safriua, and sulphur 
are especially recommended for cases occurring in women; 
aurum, benzoin, causticum, and many other drugs are sympto- 
matically indicated at times. Acute exacerbations are bene- 
fited by colchicine. Ferrum iodide may be tried in the form of 
the syrup. 



358 CONSTITUTIONAL DISEASES. 

RICKETS. 

(Rachitis.) 

Etiology. — This nutritional disease of childhood is due to im- 
proper feeding and insanitary surroundings, and in conse- 
quence it is found principally in the children of the tenements 
in large cities. 

Pathology. — The characteristic lesion is an increased produc- 
tion of cartilage at the epiphyses and excessive cell-growth 
beneath the periosteum, with slow or arrested ossification, 
whereby the bones become unnaturally flexible and deformed. 
There is a decided deficiency of lime salts in the bones. The 
liver and spleen are enlarged, and catarrhal inflammations of 
the respiratory and gastro-intestinal tracts are common. 

Symptoms. — In a child, usually less than two years of age> 
mild symptoms of ill-health, such as restless sleep, digestive 
and nervous disturbances, and excessive sweating about the 
head, may attract attention. Delayed dentition and muscular 
weakness may also be noticed. On examination the charac- 
teristic " rickety" condition is found; the head is large in pro- 
portion to the face, or the ribs are beaded (rachitic rosary), 
the knees are bent or bowed, the spine curved, the belly 
prominent, and the skin pale. Convulsions, tetany, and 
laryngismus stridulus are not uncommon occurrences in these 
children. 

Complications. — The rickety child is weak and therefore pe- 
culiarly susceptible to all the ills of childhood, especially bron- 
chitis, broncho-pneumonia, pulmonary collapse, and diarrheal 
troubles. 

Prognosis. — The disease in itself is not fatal, and if complica- 
tions can be avoided the course, though prolonged over 
months, tends toward recovery. The deformities are, how- 
ever, persistent. 

Treatment. — See that the child is properly housed, fed,, 
bathed, aired, etc., and prescribe such medicines as phosphorus y 



CONSTITUTIONAL DISEASES. 359 

calcarea phos., calcarea carb., ferritin phos., phosphoric acid, 
silica, etc. Orthopedic apparatus or even surgical operation 
may be necessary to straighten the distorted bones. 

OSTEOMALACIA. 

(Mollities Ossiura; Malacosteon.) 

Etiology. — The causes of this rare affection are little under- 
stood. It occurs principally in women, especially in connec- 
tion with pregnancy and lactation; a smaller proportion of 
cases' may be attributed to starvation, and a few to senility. 
The disease appears to be common in certain geographical 
locations. 

Pathology. — The calcium salts of the bones are absorbed by 
the fluids of the body, being found in increased proportion in 
the blood and excretions; and as a consequence the bones be- 
come softened and distorted, the pelvis in particular being de- 
formed and narrow. 

Symptoms.— -The onset is attended with pain of a rheumatoid 
type in the portion of the body first attacked, and after a time 
deformity becomes apparent, the bones being twisted or 
bent. Fractures may result from slight traumatism, and, refus- 
ing to reunite, may form false joints. 

Prognosis. — Recovery is rare, although the disease pursues a 
chronic course and death may be deferred for five or ten years. 
Temporary arrests may occur. 

Treatment. — Attention should be directed to the patient's 
hygiene; she should have an abundance of good food, and 
pregnancy must be avoided. Phosphorus is the principal 
remedy, although the calcareas and other nutritional remedies 
should be considered. 

OBESITY. 

(Polysarcia; Adipositas Universalis.) 

Etiology. — The abnormal accumulation of fat throughout the 
body appears to be the result of impaired oxidation. Factors 



360 CONSTITUTIONAL DISEASES. 

favoring it are heredity, over-eating of either carbohydrates, 
fats, or proteids, and muscular inactivity. Anemia and chloro- 
sis favor the accumulation of fat through defective oxidation, 
and sexual continence also contributes to it. 

Symptoms. — The increased bulk of the patient, which is seen 
at a glance, renders his movements sluggish and his gait wad- 
dling. In time the fat interferes mechanically with the heart 
and with respiration, inducing dyspnea. Cardiac hypertrophy 
may ensue, but later fatty infiltration of the myocardium leads 
to failure of the heart, and arterio-sclerosis, interstitial ne- 
phritis, or diabetes mellitus may be added. 

Prognosis. — While corpulence may not be incompatible with 
long life, it tends to produce the pathological conditions noted. 
Recovery is quite generally possible, however, provided the 
patient will persist in the somewhat irksome treatment. 

Treatment. — 1. Limit the ingestion of fat-producing food. 
Cut down the allowance of all food, but especially that of 
carbohydrates, and allow only a small quantity of fluid with 
meals. 

2. Promote oxidation. Exercise, in the form of gymnastic 
work, walking or climbing, and bicycling, together with mas- 
sage and Turkish or steam baths, accomplishes this purpose. 

The administration of drugs is not advisable. 



DISEASES OF THE NERVOUS 
SYSTEM. 



Disease of the nervous system manifests itself by disorders 
of intellection, of sensation, of muscular action, of reflex 
action, or by vasomotor or trophic disturbances. 

Disorder of the intellectual functions may occasion loss of 
memory, disturbed sleep, hallucinations or delusions, delirium 
or coma, and various abnormalities of speech. Disturbances 
of sensation may lead to diminution of sensibility (anesthesia), 
increase of sensibility (hyperesthesia), or abnormal sensations 
(paresthesia). The skin may be disordered as to the sense of 
touch, of locality, of position, of pressure, of temperature, or 
of pain. Abnormalities of muscular action are manifested in 
paralysis, in spasm or convulsion, or inco-ordination. 

Disorder of the reflexes is rarely discovered until some of 
the symptoms already mentioned have led to their investiga- 
tion. Vasomotor disturbances may be evidenced by abnormal 
redness or pallor of the skin; and trophic disorders lead to 
wasting of certain portions of the body. 

Interrogation of the Patient. — Attention having been attracted 
by phenomena suggesting disease of the nervous system, certain 
questions concerning heredity, environment, habits, and pre- 
vious disease become of extreme importance. The patient 
should be questioned as to: 

1. His family history. Have there been mental diseases, 
chorea, convulsions, or paralysis ? 

2. His personal history. Has he ever suffered from rheu- 
matism, gout, syphilis, or alcoholism ? 

3. His work. Is he exposed to noxious influences or poisons, 
such as lead, mercury, or arsenic ? 



362 DISEASES OF THE NERVOUS SYSTEM. 

4. His environment. His home surroundings, etc. 

5. His habits, as to eating, sleeping, stimulants, venery^ 
work, and recreation. 

6. In cerebral cases: Has there been any discharge from 
the ear? Any injury to the head? 

7. If there have been convulsions, inquire as to: His age at 
the time of the first convulsion, and the circumstances sur- 
rounding it. The supposed cause. Describe in detail the first 
attack. When did the second occur ? What has been the 
longest and what the shortest interval between the attacks ? 
Are they more, or less, frequent now ? Do they occur during 
sleep ? Has he any aura ? If so, what and where ? Is the 
onset sudden or gradual? Does he remain rigid, or does he 
struggle? Are the convulsive movements uni- or bilateral?' 
Where do they begin ? Does he bite his tongue, urinate, or 
defecate during the seizure ? Has he ever hurt himself during 
the attack ? How does it end ? Are there any after-symptoms, 
such as sleep, headache, or automatism ? 

8. If there be paralysis ascertain its exact location. Did he 
have any premonitory symptoms before the onset? Did it 
develop abruptly or gradually? Was he unconscious at the 
time; and if so, for how long? Has he any headache? Where 
is it situated ? Is it worse at night? Has he any giddiness? 
Any difficulty in walking ? Inquire carefully for any symp- 
toms of heart or kidney disease. 

EXAMINATION OF THE NERVOUS SYSTEM. 

The close association of nervous phenomena with every dis- 
ease of the human body renders it absolutely essential that 
knowledge of the condition of each important organ, as well 
as whatever information may be derived from investigation of 
the various excretions, shall be in the possession of the phy- 
sician before he formulates an opinion as to the case. Exami- 
nation of the thoracic and abdominal viscera, and of the 
urine, stomach-contents, or blood, should, therefore, in many 



DISEASES OF THE NERVOUS SYSTEM. 363 

cases precede the special examination directed to the nervous 
system. By means of the latter he must, moreover, determine 
two points: 

(1) The nature of the lesion; and 

(2) Its localization. For this purpose a certain degree of 
familiarity with the anatomy and physiology of the nervous 
system is necessary. 

I. THE INTELLECTUAL FUNCTIONS. 

As a rule the mental condition can be judged with fair ac- 
curacy while obtaining the history of the case. Note, in the 
first place, whether the patient is right or left-handed. Test 
his memory by asking him what day of the week it is, or what 
he had for breakfast. Inquire as to how he sleeps. Note his 
emotional condition, whether excited, irritable, or inclined to 
burst into tears. Ascertain whether any hallucination or de- 
lusion is entertained. The presence of delirium or stupor 
will, of course, prevent this investigation. 

Notice his speech. Does he stammer? Does he speak 
deliberately, as though scanning a line of poetry (dissemi- 
nated sclerosis); or does he slur his words like a drunken man 
(paresis)? These are disorders of articulation (dysarthria, 
anarthria) and may be due to lesions of the muscles, their 
nerves, or of the latter's nuclei of origin. 

If it is not articulation but the ability to speak at all, or else 
to understand speech when written or spoken, that is dis- 
ordered, the condition is due to a cerebral lesion and is known 
as aphasia. The cerebral speech mechanism consists of: 

(1) Two receiving portions, one for written and one for 
spoken speech; and, 

(2) Two producing portions, one for speaking and the other 
for writing. 

Failure of the receiving portion {sensory aphasia) may, 
therefore, be visual {word blindness) or auditory {ivord deaf- 
ness) ; and failure of the producing mechanism is evidenced 



364 DISEASES OF THE NERVOUS SYSTEM. 

by motor aphasia, with inability to talk {ap hernia) , inability 
to write {agraphia), or inability to use the sign language 
{amimid). Two or more of these conditions are associated in 
most cases. 

Localization. — The site of the lesion producing motor aphasia 
is about the third frontal convolution (Broca's); that of sen- 
sory aphasia is in the neighborhood of the first frontal con- 
volution. In right-handed subjects the lesion is on the left 
side of the brain; in the left-handed it may be on the right 
side. 

The lesions producing aphasia are of many kinds, among 
the more important being intracranial tumor, abscess, gumma, 
thrombosis, embolism, softening, and depressed fracture of 
the skull. Occasionally it is without organic cause, being due 
to hysteria, epilepsy, migraine, or other neurosis. 

Tests. Having found the patient to be in some degree in- 
capable of voluntary utterance, discover whether his hearing 
is good. If it is, ask him to put out his tongue or close his 
eyes, and to whistle or to smile. If he does not do these 
things, there is zvord-deafness. 

Show him some common object, such as a pen or a book, 
and ask him to name it. If he cannot, he forgets some words 
{amnesic aphasia). If he applies the wrong name, calling 
the pen a book or vice versa, he has paraphasia. 

Ascertain if his sight is good. If it is, write on a piece of 
paper some simple question, such as "How old are you?" 
If he does not reply satisfactorily, there is word-blindness. 

Ask him to write his name (if he has word-deafness, put the 
question in writing), and if he does so, test him further with 
some simple question. If he writes a satisfactory reply, there 
is no agraphia. Ask him to write a short account of his ill- 
ness and note whether he uses the wrong word at times 
{paragraphia ) . 

Ask him to copy a simple sentence from a book. If he does 
so, ascertain if possible whether he understands its meaning. 
If he does not, he has alexia. 



DISEASES OF THE NERVOUS SYSTEM. 365 

Note whether he nods his head for "y es " and shakes it for 
" no." Loss of this sign language is termed amimia; or if he 
misuses the gesture, shaking his head when he means "yes," 
there is paramimia. 



II. CRANIAL NERVE FUNCTIONS. 

1. First or olfactory nerve. Apply to each nostril 
separately two small bottles containing respectively oil of 
peppermint and tincture of asafoetida, and ask the patient if 
he recognizes the difference. There may be a loss of the sense 
of smell {anosmia), increased sensitiveness of smell {hyper- 
osmia), perversion of the sense of smell, in which, for ex- 
ample, offensive odors seem pleasant {parosmia), and there 
may be hallucinatiens of smell (occurring sometimes as an 
epileptic aura). 

2. Second or optic nerve, {a) Test the visual acuity of 
the patient by means of the ordinary Snellen types; if, for in- 
stance, at a distance of 10 feet he is able to read only the type 
normally visible at 20 feet, his vision is recorded as yrr; if he 
is able to read that normally visible at 15 feet, his vision is xr> 
and so on. 

If acuity of vision is much diminished, place him with his 
back to the light and hold up in front of him different numbers 
of fingers, asking him how many he sees. If there is a ques- 
tion as to whether he can distinguish light from darkness, test 
him by flashing light into his eyes with a head-mirror, asking 
him to say when it is dark and when light. 

There may be defective vision without change in the fundus 
{amblyopia), or defective vision in one eye due to a lesion in 
the opposite side of the brain {crossed amblyopia), and there 
ma} T be complete blindness without ocular change {amaurosis). 

{b) Test the field of vision by sitting in front of the patient, 
having him place his hand over one eye and keep the other 
eye fixed on the examiner's face; and then bring some object, 
such as a pencil or a finger, gradually into his field of vision, 



366 DISEASES OF THE NERVOUS SYSTEM. 

first from one side, then the other, then from above, and finally 
from below. More accurate results may be had by using the 
perimeter. 

The field of vision may be contracted all around the peri- 
phery {concentric contraction*) as in hysteria, optic atrophy, 
and retinal disease. Vision may be lost in the centre of the 
field {central scotoma) as the result of retrobulbar neuritis, 
which is usually bilateral, or because. of disease of the choroid 
or retina, when it may be unilateral. Finally, there may be 
loss of sight in one-half of the field of vision in both eyes 
{hemianopsia)', this may affect the temporal half of each 
field {temporal hemianopsia), it may affect the nasal halves 
{nasal hemianopsia) or it may affect corresponding sides of 
each eye {homonymous hemianopsia). 

The color field may be tested in a somewhat similar fashion, 
using blue, yellow, red, and green cards. Normally the blue 
field is largest, the others following in the order named. Con- 
centric contraction of the color field occurs in hysterical ambly- 
opia. Color blindness invalidates the test; to discover it, let 
the patient attempt to match skeins of wool of different colors 
in good daylight. 

3. The motor nerves of the eye (third, fourth, and sixth) 
should be tested together. A lesion of any one of them may 
produce (1) strabismus, (2) defective power of ocular move- 
ment, (3) diplopia. Inability to move the eye outwards, with 
diplopia on looking in that direction and possibly internal 
strabismus, indicates paralysis of the external rectus muscle 
{sixth nerve). If downward movement is impaired, with 
diplopia on looking down and possibly convergent strabismus, 
there is paralysis of the superior oblique {fourth nerve). If 
there is utter loss of movement except outwards and a little 
downwards, with ptosis, immobile pupil, and loss of accommo- 
dation, there is complete paralysis of the third nerve. The 
paralysis may, however, be partial, only one or two of the 
functions being abolished. 

Tests {a). Place the patient with his back to the light and, 



DISEASES OF THE NERVOUS SYSTEM. 367 

standing in front of him, direct him to follow with his eyes the 
movements of one of the examiner's fingers. Notice whether 
this action develops a squint in either eye; and repeat the test 
on each eye separately, noting its motility in every direction. 
Notice whether a squint is constantly present, even when the 
patient looks straight ahead, and whether it follows the sound 
eye equally in all its movements; if so, it is a concomitant 
{spasmodic) strabismus. If, on the other hand, the affected 
eye fails to follow the sound one when the patient attempts*to 
turn it in the direction of action of the paralyzed muscle, it is 
a paralytic strabismus. Diplopia is usually present in the 
latter form only. 

(b) Defective power of convergence of the eyes is ascer- 
tained by holding the finger about 18 inches in front of the 
patient's nose, telling him to keep looking at it. Gradually 
bring it nearer to his nose, and notice whether the eyes re- 
main directed towards each other or whether they tend to 
diverge after first converging. 

(e) Diplopia occurs in recent strabismus, but when the 
latter is of long duration the patient learns to disregard the 
false image and takes cognizance of only the true. In these 
chronic cases the false, image may be restored by placing a 
piece of colored glass before one eye, preferably the sound 
one, when the false image will be seen at one side of the true 
one. Let the patient alternately close each eye; if the image 
to the right be that seen with the right eye, the diplopia 
is simple {direct or homonymous), but if the image to the 
right is seen with the left eye there is crossed diplopia. 

Diplopia not dependent on eye disease is usually significant 
of serious nervous diseases (meningitis, tumor, abscess, dis- 
seminated sclerosis, syphilis). It may occur transiently, 
however, in alcoholic intoxication or cerebral concussion. 

id) Abnormal ocular movements. Ask the patient to look 
straight ahead, and then observe whether the eyes remain 
steady. Tell him to look to the extreme right, then to the ex- 
treme left, then upwards, then downwards; if rhythmical 



368 DISEASES OF THE NERVOUS SYSTEM. 

oscillations of the eyeball are detected, there is nystagmus. 
The presence of this symptom is pi oof positive of organic dis- 
ease (disseminated sclerosis, intracranial tumor, meningitis, 
etc.). 

Note if the head and eyes are kept persistently turned to 
one side {conjugate deviation) . If this be due to paralysis and 
the lesion be in the cerebral hemisphere, the eyes turn towards 
the side of the lesion. If, however, the lesion be irritative 
rather than paralytic, the deviation is towards the healthy 
side. If the lesion be in the pons, these conditions are exactly 
reversed. 

Examination of the pupils, (a) Compare the size of the 
two pupils, first in a bright light and then in a dim one. Note 
whether they are small or large, and whether irregular in out- 
line. Irregularity of the shape of the pupil may be due to ad- 
hesion of the iris to the lens, or perhaps be an early symptom 
of paralytic dementia. 

(/;) Mobility. Place the patient so that he faces a bright 
light, and cover each eye with a hand for half a minute. 
Withdraw one hand suddenly and watch the pupil; it should 
contract almost immediately and then after slight oscillation 
settle down to its normal size {reaction to light). Test each 
eye separately in this fashion. 

Hold one finger near the patient's nose while he looks at a 
distant object, then suddenly tell him to look at the finger. 
As he does so, the pupils become much smaller {reaction to 
accommodation) . 

The pupil may react to accommodation but not to light 
{Argyll-Robertson pupil), indicating a lesion interrupting the 
reflex path between the optic nerve and the nucleus of the 
third nerve (locomotor ataxia, paretic dementia, etc.). If the 
pupil reacts neither to accommodation nor light, there is prob- 
ably a lesion of the pupillary centre or the third nerve. 

Fifth Nerve. — The trigeminus is a mixed nerve which 
supplies by its motor trunk the masticatory muscles, and by 
its sensory portion the skin of the face, the mucous membrane 



DISEASES OF THE NERVOUS SYSTEM. 369 

of the mouth and nasal cavity, the conjunctiva, the cornea, 
and the anterior tongue with gustatory fibres (via chorda 
tympani), and the nose with olf actor} 7 fibres. It may be af- 
fected by lesions of the pons (hemorrhage, sclerosis) by in- 
jury or disease at the base of the. skull, or by pressure upon or 
inflammation of its opthalmic, superior maxillary, or inferior 
maxillary divisions. The sensory portion may also be affected 
in hysteria, and by lesions of the posterior portion of the in- 
ternal capsule; and the gustatory fibres may be influenced by 
facial lesions involving the chorda tympani. 

Paralysis of the nerve, if complete, occasions loss of sensa- 
tion in the areas of the skin and mucous membranes men- 
tioned, together with difficulty in chewing. Trophic lesions 
may affect the cornea, and the salivary, buccal, and lachrymal 
secretions may be diminished. Spasm of the muscles of masti- 
cation {trismus) occurs in tetanus and other diseases; clonic 
spasm is exemplified in " chattering teeth." Irritation of the 
nerve may occasion facial neuralgia, and at times pain may be 
due to actual neuritis. This is frequently the case when in- 
flammatory processes affect the orbit, antrum, or jaws. 

Tests.— Motor functions, (a) Place the hands first on the 
temporal and then on the masseter muscles while the patient 
clenches his teeth. They should stand out with equal promi- 
nence on the two sides, but this will not occur on a paralytic 
side. There may be deviation of the jaw toward the paralyzed 
side on opening the mouth. 

(b) Sensory functions. The common sensibility of the area 
supplied by the nerve is tested in the usual way. (See exami- 
nation of the Sensory Functions.) Examine also the sense 
of taste. Use the following solutions: Sodium chloride (10%); 
tartaric acid (10%; ; strychnine sulphate (1-100); saccharine 
(1-250). 

Ask the patient to put out his tongue and keep it out until 
the test is ended. Place the saccharine solution on the tongue, 
asking, "Is it sour?" If the taste is normal he will shake his 
head. Proceed in the same way with the other solutions, ask- 

21 



370 DISEASES OF THE NERVOUS SYSTEM. 

ing him, for instance, if the tartaric acid is sweet or bitter, 
etc. 

A weak galvanic current may be used, as it occasions a me- 
tallic taste under normal conditions. 

Seventh nerve. The facial is the motor nerve of the face; 
it may be paralyzed (Bell's palsy) as the result of lesions in 
its nucleus, its cortical centre, or its trunk. As a result the 
face is drawn to the sound side, and the paralyzed side is 
smoothed of all its wrinkles, the eye cannot be completely 
closed, and the patient is unable to whistle. 

Tests, {a) Ask the patient to close his eye as tightly as 
possible. Note that the upper lid droops as though heavy, 
while the eye is turned upward and quite a space remains un- 
covered Try to open the eye with the fingers while the 
patient endeavors to keep it closed; with the healthy eyelid 
this is very difficult, but when paralysis is present the eye may 
be opened quite easily. 

(&) Ask the patient to whistle. He cannot. 
(c) Ask him to smile. The mouth becomes drawn only to. 
the healthy side. 

Localizatio?i of the Lesion. Cerebral or supra-nuclear pa- 
ralysis effects chiefly the lower part of the face. In peripheral 
or infra-nuclear paralysis the upper and lower portions are 
equally involved. A lesion of the nerve before it enters the 
aqueduct causes paralysis of the stapedius muscle, whereby 
the patient becomes extremely sensitive to loud sounds. A 
lesion within the aqueduct, except its outer end, involves the 
fibres of the chorda tympani and produces a paralysis of taste 
sensation in the anterior two-thirds of the tongue. It is nec- 
essary, therefore, to inquire as to the patient's sensitiveness to 
loud sounds, and to test his sense of taste as described in con- 
nection with the fifth nerve. 

Spasmodic movements of the muscles supplied by the 
seventh nerve (facial spasm, convulsive tic) may include all 
the muscles, or only certain groups (e. g., blepharospasm). 
Eighth nerve. The auditory nerve consists of two sets of 



DISEASES OF THE NERVOUS SYSTEM. 371 

fibres, one of which supplies the cochlea, subserving the hear- 
ing, and the other supplies the vestibule and semi-circular 
canals, having to do with equilibration. The nerve may be 
affected anywhere in its course; in the cortical auditor centre 
(in the first temporo-sphenoidal convolution), in the nucleus 
about the floor of the fourth ventricle, in its course at the base 
of the brain, within the internal auditory meatus, or in its ter- 
minal filaments. 

a. The sense of hearing may be (1) lost {nerve deafness) ; 
(2) hyperacute, so that even slight sounds are heard with pain- 
ful intensity {auditory hyperesthesia, hyperacusis)\ this occurs 
in hysteria and in lesions of the facial nerve above the aque- 
duct, or (3) accompanied by subjective auditor) 7 sensations, 
such as "ringing in the ears" {tinnitus). 

Tests. — (a) Exclude the presence of wax in the ear. Stand 
behind the patient and holding a watch at some distance from 
his ear, outside of the normal hearing range, bring it grad- 
ually nearer and ask him to speak when he hears it tick. Test 
each ear separately, the other being closed. It is necessary, 
of course, to know at what distance the watch used is heard 
by a healthy ear. 

{b) If hearing is defective, decide whether it is due to a 
lesion in the nerve or in the middle ear. In order to do this, 
strike a tuning-fork and place its end against the middle of 
the patient's forehead. If the deafness is due to disease of 
the middle ear the patient will hear the tuning-fork louder on 
that side than on the healthy one, but if the deafness is due 
to auditory nerve disease the sound will be heard only on the 
healthy side. Deafness is probably due to nerve disease if 
hearing is better in a quiet place, if conversation is heard 
better than a watch, or if inflation of the middle ear renders 
the hearing worse. 

b. Equilibration may be disordered, with resulting vertigo. 
In true vertigo external objects seem to move around the 
patient. The association of vertigo with deafness and tin- 
nitus aurium constitutes the disease known as labyrinthine 
vertigo or Meniere ' s disease. 



372 DISEASES OF THE NERVOUS SYSTEM. 

It must be remembered that vertigo ma} 7 also be the result 
of disease elsewhere in the auditory apparatus, to an ocular 
palsy, to loss of muscular sensibility in the lower extremities, 
and to cardiac, gastric, and renal diseases. 

Ninth nerve. The glosso-pharyngeal supplies sensibility 
to the posterior third of the tongue and to the mucous mem- 
brane of the pharynx; motion to the stylo-pharyngeus and the 
middle constrictor of the pharynx; and the sense of taste to 
the posterior part of the tongue. This nerve has numerous 
communications, especially with the tri-facial, the facial, and 
the pneumo gastric nerves, and is rarely paralyzed alone. 
Symptoms of such a paralysis would be loss or perversion of 
the sense of taste and difficult deglutition. 

Tests.— {a) Examine the sense of taste in the posterior part 
of the tongue. 

(/;) Tickle the back of the pharynx and notice whether the 
reflex is present. 

Tenth nerve. The pneumogastric or vagus is a mixed 
nerve of motion and sensation, some of its most important 
motor fibres being derived from the spinal accessory. The 
nerve is distributed to the pharynx, larynx, esophagus, trachea, 
lungs, heart, stomach, intestines, and spleen. It may be 
affected by lesions in the nucleus or in the nerve trunk. 

Tests.— -1. (a) The pharynx. Ascertain whether the patient 
has difficulty in swallowing. If paralysis is present, he 
usually complains of regurgitation of food through his nose or 
entrance of food into the larynx. 

(b) Ask him to pronounce words which require complete 
closure of the naso-pharynx. If the paralysis is bilateral he 
is unable to do so, and "egg" becomes "eng" and "rub" be- 
comes " rum." 

(c) Examine the pharynx, using a tongue depressor, and 
note whether both sides of the palate arch upwards when the 
patient says "ah." 

2. The larynx. Examine with the laryngoscope. Tell the 
patient to take a deep breath, and note whether the vocal 



DISEASES OF THE NERVOUS SYSTEM. 373 

chords become more widely separated, as they should in health. 
If, instead, they come more closely together during inspiration, 
there is total abductor palsy, often due to central disease; or 
one cord may be normal, but the other lies near the middle 
line and does not move during inspiration — unilateral abductor 
palsy. 

If the cords are normal in position and move normally in 
respiration, but are not brought together by the attempt at 
phonation, there is adductor paralysis. One cord may be 
moderately abducted and motionless while the other moves 
freely and even beyond the middle line in phonation — total 
unilateral palsy. Or both cords may remain moderately ab- 
ducted and motionless — total bilateral palsy. 

Paralysis of the vocal cords may be peripheral in origin, due 
to pressure on the recurrent laryngeal (by goitre, aneurism, 
tumors of the mediastinum, or pericarditis) or to neuritis; it 
may be central, as in hysteria; or nuclear, due to involvement 
of the nucleus of the accessory nerve in the floor of the fourth 
ventricle (bulbar paralysis, disseminated sclerosis, locomotor 
ataxia, syringomyelia, etc.). 

It must be remembered that the laryngeal motor fibres of 
the pneumogastric are all derived from the spinal accessory, 
and that lesions of the latter before its junction with the 
pneumogastric may occasion laryngeal paralysis. 

Eleventh nerve. The spinal accessory nerve is purely 
motor. One portion of it supplies the laryngeal muscles 
through the pneumogastric, as has been described. The 
other portion of it is distributed to the sterno-cleido-mastoid 
and trapezius muscles, which may be paralyzed by lesions 
of that portion. 

Tests. — 1. Paralysis of one sterno-mastoid occasions diffi- 
cult}' in rotating the head to the opposite side. 

2. Paralysis of the trapezius may be detected by pressing 
upon the patient's shoulders while he tries to shrug them. 

Twelfth nerve. The hypoglossal is the motor nerve of 
the tongue, and also supplies the depressors of the hyoid bone 



374 DISEASES OF THE NERVOUS SYSTEM. 

It arises beside the olivary body in the medulla, and may be. 
involved in disease of the cortex (cerebral hemorrhage, throm- 
bosis, embolism, etc.), or of the nucleus (bulbar palsy, loco- 
motor ataxia), or its fibres may be damaged in their course 
to the periphery. 

Test. — Ask the patient to protrude his tongue as far as pos- 
sible. Hypoglossal paralysis is indicated when the tongue, 
instead of being put out straight, deviates toward the paralyzed 
side. The apparent deviation of the tongue which appears 
when one side of the face is paralyzed must be distinguished 
from the true glossal paralysis just described. 

In nuclear disease the palsy is apt to be bi-lateral, and in 
consequence the tongue lies motionless in the floor of the 
mouth. Note whether the tongue is atrophied; the latter 
condition indicates a nuclear or infra-nuclear lesion. Note if 
there be any tremor or spasm of the tongue. 

III. MOTOR FUNCTIONS. 

Examination of the motor functions implies investigation as 
to: 

1. The existence of muscular paralysis or weakness. 

2. The state of muscular nutrition. 

3. The co-ordination of muscular action. 

4. The occurrence of abnormal muscular movements. 

1. Muscular power. Note the patient's ability to perform the 
ordinary muscular movements, such as walking or sitting up 
in bed. Note whether he can move each of his extremities. 
Having in this way detected any gross defects of motility, ex- 
amination should be directed to the principal muscles and 
groups of muscles separately. The patient is asked to throw 
into action the iriuscle or muscle-group which is undergoing 
investigation, and while he does so the examiner interposes a 
certain degree of passive resistance to the action. If by this 
test a muscle or group of muscles is found to be feeble, the 
condition is described as a paresis ; if voluntary motion is lost, 



DISEASES OF THE NERVOUS SYSTEM. 375 

it is said to be a paralysis. When the presence of a motor 
defect has been determined, its degree and distribution must 
be ascertained; and for this purpose each movement — abduc- 
tion, adduction, extension, and flexion — should be tested 
separately on the two sides of the body and compared, due 
allowance being made for the superior strength usually found 
on the right side. If the patient is unconscious, raise each 
limb separately and allow it to fall upon the bed; as a rule, 
the paralyzed limb drops limp and helpless, while the un- 
affected one offers slight resistance. It may be found that the 
paralysis is confined to the muscles supplied by a single nerve, 
e. g. y the musculo-spiral, or to a spinal segment, or it may 
constitute a hemiplegia, paraplegia, or monoplegia. 

The power of individual muscles may be tested as follows 
(Butler), their innervation and their representation in the 
spinal segments being indicated in parenthesis: 

(i) Neck Muscles. Practically the sterno-cleido-mastoid alone is exam- 
ined. If the patient is lying down, request him to raise his head; or if he 
is sitting up, to turn the head as far as possible to the right and left, with or 
without resistance offered by applying the hands to the sides of the head; or 
to bend it forward against pressure on the forehead. If the muscle is not 
paralyzed it stands out prominently. (Spinal accessory nerve; medulla and 
second and third cervical segments.) 

(2) Muscles of the Upper Extremity. Deltoid. — Request the patient to 
raise the arms laterally to a horizontal position. Inability to do so indicates 
deltoid paralysis. (Circumflex nerves; fourth, fifth, and sixth cervical seg- 
ments.) 

Pectoral Muscles. — Stretch out the arms straight in front, and then ap- 
proximate the hands against resistance by the examiner, meanwhile watch- 
ing both heads of the pectoral muscle. (Anterior thoracic nerve; fifth, 
sixth, and seventh cervical segments. ) 

Latissimus Dor si. — Raise the arms laterally to a level; then, while keep- 
ing them fully extended, bring the arms downward and backward, as if to 
make the hands meet behind the sacrum. The examiner standing behind 
the patient resists the movement. (Subscapular nerves and branches of 
dorsal and lumbar nerves; sixth and seventh cervical segments.) 

Serratus Magnus. — Desire the patient to push with his hands against 
those of the examiner. If the serratus has lost its power the scapula will pro- 
ject, and the digitations of the muscle, which ordinarily should be visible, 
will not be seen. (Posterior thoracic nerve; fifth and sixth cervical seg- 
ments.) 



376 DISEASES OF THE NERVOUS SYSTEM. 

TTCipezius. — Ask the patient to raise the shoulders as close to his ears as 
possible against the resistance of the examiner's hands. This will demon- 
strate the strength of the upper part of the trapezius. The middle and lower 
portions are tested by desiring him to bring the scapulae as close together as 
possible. (Spinal accessor}^ nerve; medulla and second and third cervical 
segments. ) 

It is hardly possible to detect paralysis of the levator anguli scapulae and 
rhomboids unless the trapezius is also involved. 

Biceps. — Let the patient flex his extended arm, his elbow resting on the 
observer's left hand, while the latter's right hand, grasping the wrist of the 
patient, offers the necessary resistance. Also supinate the hand against re- 
sistance. (Musculo-cutaneous nerve; fourth, fifth, and sixth cervical seg- 
ments.) 

Triceps. — The triceps may be tested as is the biceps, excepting that the 
previously flexed arm is to be extended against resistance. (Musculo-spiral 
nerve; sixth, seventh, and eighth cervical segments.) 

Supinator Longus. — Test as for the biceps, except that the hand should 
be midway between supination and pronation. If the muscle is paralyzed,, 
it will fail to become conspicuous on the radial side of the upper part of the 
forearm. (Musculo-spiral nerve; fourth and fifth cervical segments.) 

Flexors of the Wrist. — Grasping the patient's hand, the palm being up- 
ward, desire him to bend the hand up toward his forearm against resistance. 
(Median and ulnar nerves; eighth cervical segment.) 

Extensors of the Wrist. — The patient's hand being held palm downward, 
he is required to bend it backward against resistance. Moderate weakness 
of the extensors of the wrist may be manifested by asking him to squeeze 
the examiner's hand, in which case the wrist will become involuntarily 
flexed, the weakened extension being unable to counteract the flexors. 
Marked or complete paralysis of the extensors causes "wrist-drop." (Muscu- 
lo-spiral nerve; seventh cervical segment.) 

Flexors of the Fingers. — Because of the usual difference in the strength of 
the two hands, the examiner should cross his forearms and place his right 
hand in the right hand of the patient, and vice versa. Then let the patient 
squeeze his hands. If the observer keeps his own fingers extended and 
bunched loosely together, he will be able to withstand a very hearty grasp 
without discomfort. (Median and ulnar nerve; eighth cervical segment.) 

Adductor Pollicis. — Ask the patient to pinch, with his thumb and fore- 
finger, one of the examiner's fingers. (Ulnar nerve; eighth cervical seg- 
ment.) 

Opponens Pollicis. — Desire the patient to approximate the ends of the 
little finger and the thumb. (Median nerve; first dorsal segment. ) 

The interosseous and lumbrical muscles of the hand flex the proximal 
phalanges, and extend the middle and terminal phalanges. The dorsal in- 



DISEASES OF THE NERVOUS SYSTEM. 377 

terossei abduct, the palmar adduct, the fingers from and toward a longitud- 
inal line down through the centre of the middle finger. Test by making the 
patient separate and approximate the fingers, and flex the proximal pha- 
langes, keeping the middle and terminal phalanges extended. Paralysis of 
these muscles causes the " claw-hand." (Ulnar and median nerves; eighth 
cervical and first dorsal segments.) 

(3) Trunk muscles. Paralysis of the diaphragm is indicated by absence 
of the protrusion of the epigastrium, which is normally seen during in- 
spiration; instead of protruding, the epigastric region and upper abdominal 
walls often appear to be sucked in during inspiration. ( Pneumogastric 
nerve and phrenic plexus of the sympathetic. ) 

The erector muscles of the spine are examined by having the patient lie 
face downward, and asking him to raise the head and shoulders without as- 
sistance from the hands. Unless paralyzed, the erectors become plainly 
visible during the attempt. (Dorsal nerves; second to twelfth dorsal seg- 
ments.) The abdominal muscles are tested in a similar manner, except that 
the patient lies in the dorsal position while making an effort to raise the 
head. (Six lower dorsal nerves and lumbar plexus; seventh dorsal to fourth 
lumbar segments.) 

(4) Muscles of the Lower Extremity. Flexors of Thigh.— The patient 
lying upon his back, ask him to raise the leg up from the bed, the knee be- 
ing kept straight. This determines the strength mainly of the ileo-psoas, 
partly of the quadriceps. (Crural nerve of lumbar plexus; third and fourth 
lumbar segments. ) 

Extensors of the Thigh. — The leg being kept straight and the patient 
upon his back, raise the foot and ask him to bring it down upon the leg" 
against resistance. This determines the strength of the gluteus maximus 
and partly of the hamstring muscles. (Superior and inferior gluteal nerves, 
first and second sacral segments; and the sciatic nerve, fifth lumbar seg- 
ment. ) 

Abductors of the Thigh. — Carry the leg across the middle line, and desire 
the patient to force it toward the outer side against resistance, thus testing 
mainly the gluteus medius. (Superior gluteal nerve from the sacral plexus;, 
first and second segments. ) 

Adductors of the Thigh. — Carry the leg outward and desire the patient to 
force it back to the middle line against resistance, thus testing the adductors 
longus, brevis, and magnus. (Obturator, great sciatic and crural nerves; 
from lumbar plexus.) 

In-rotators of the Thigh. — With the patient lying face downward, flex the 
knee to a right angle, grasp the foot, and oppose resistance while he in- 
rotates the thigh. This tests mainly the gluteus minimus. (Superior gluteal 
nerve from the sacral plexus. ) 

Out-rotators of the Thigh. — Test the power of out-rotation in similar 



378 DISEASES OF THE NERVOUS SYSTEM. 

fashion, thus determining the condition of the pyriformis, getnelli, quad- 
ratics femoris, and obturators. (Sacral and lumbar plexus. ). 

Flexors of Knee. — With the patient lying face downward, or even while he 
sits in a chair, let him bend the knee while the examiner resists the move- 
ment by pressure against the heel. This tests mainly the biceps, semi-mem- 
branosus, and semi-tendinosus. (Sciatic nerve; fifth lumbar segment ) 

Extensors of Knee. — With the patient in the dorsal position, flex the knee 
and by pressure upon the sole of the foot resist his endeavor to extend the 
knee, thus testing principally the quadriceps femoris. (Crural nerve; third 
lumbar segment. ) 

Plantar Flexors {Extensors) of the Foot. — With the leg straight, resist by 
pressure upon the sole the patient's endeavor to bring the tarsus in line with 
the leg, thus testing the gastrocnemius, soleus, peroneus longus and brevis. 
(Internal popliteal and peroneal nerves; fifth lumbar and first and second 
sacral segments. ) 

Dorsiflectors of the Foot. — With the leg straight, resist the patient's 
attempt to bend up the foot, thus testing the tibialis anticus and the peroneus 
tertius. Marked paralysis of these muscles causes "foot drop." (Anterior 
tibial nerve; fifth lumbar and first sacral segments.) 

Muscles of the Foot. — The flexors, extensors, interossei, and lumbricals of 
the toes are examined in a manner similar to that applied to the hand. (Pos- 
terior tibial nerve; first and second sacral segments.) 

Paralysis. — Having ascertained by the above tests the pres- 
ence of paralysis, it becomes essential to determine its type, 
i. e., whether cerebral, due to a lesion of the upper neuron, 
or spinal, the result of disease of the lower neuron. The 
motor path consists of two segments: the upper neuron, whose 
axon leaves its cell in the cerebral cortex and joins with others 
to form the motor fibres which traverse the corona radiata, in 
ternal capsule, cms cerebri, pons, and medulla, and then for the 
most part cross to the opposite side and pass down the crossed 
pyramidal tracts to terminate in the gray matter of the anterior 
cornua; and the lower neuron, which commences in the cells 
of the anterior cornua and is prolonged as a part of a peri- 
pheral nerve to its termination in the muscles. These two 
neurons, although in close contiguity, are independent of each 
other, and the nutritional welfare of each depends entirely 
upon the integrity of its own cell body. Therefore degenera- 
tion due to disease of the upper neuron does not extend be- 
vond its own terminal fibres and the lower neuron remains 



DISEASES OF THE NERVOUS SYSTEM. 379 

intact, and vice versa. So long as the disease is limited to the 
upper neuron, the muscles undergo no wasting (except a 
slight atrophy from disuse) and the electrical reactions are not 
definitely altered. If, however, the lower neuron is affected, 
the power of movement will be absolutely lost, the muscles 
will become flaccid and atrophied, the reflexes will be lost, 
and the electrical reactions markedly changed. 

Clinically we may distinguish these two types of paralysis 
by the following signs: 

(1) The Cerebral Type, of which hemiplegia is characteristic, 
is marked by spasticity of the muscles, the limb resisting at- 
tempts at passive movement or undergoing a spasmodic con- 
traction when the latter is attempted. Contractures may 
develop; the reflexes are exaggerated, owing to absence of the 
inhibition normally exercised by the upper neuron; the elec- 
trical reactions are normal and there is no atrophy. 

(2) The Spinal Type, of which paraplegia is characteristic, is 
indicated by a flaccid state, the member being limp and the 
muscles appearing lax and offering no resistance to passive 
movement. The reflexes arc diminisJied or lost ; there is 
partial or complete loss of response to the faradic current, 
with partial or entire reaction of degeneration to the galvanic 
current; and there is marked atrophy. 

The cerebral type of paralysis is due to a lesion of the motor 
cortex, of which the pyramidal tract is an extension, and is 
usually unilateral (hemiplegia), rarely bilateral (diplegia). It 
may be due to disease of the crossed pyramidal tract in the 
cord (lateral sclerosis). The spinal type is the result of lesions 
affecting the cell-bodies in the medulla or pons (e. g., bulbar 
paralysis), of the motor cells in the anterior cornua of the cord 
(e. g., poliomyelitis), or of the peripheral nerves (e. g., 
neuritis). A mixed type may be the result of a simultaneous 
involvement of the terminals of the upper neuron and the cell- 
bodies of the lower neuron (amyotrophic lateral sclerosis, 
transverse myelitis). Functional paralysis (hysteria) is usually 
flaccid and presents neither atrophy nor the reaction of de- 



380 DISEASES OF THE NERVOUS SYSTEM. 

generation. As a rule, the history and the presence of hys- 
terical stigmata will serve to distinguish this latter condition* 

Localization and Nature of the Lesion. — Complete hemiplegia, 
unless functional, is always due to a cerebral lesion. Hemi- 
plegia with motor aphasia, in a right-handed person, is caused 
by a lesion of the third left frontal convolution or by a 
lesion in the capsule interrupting the fibres therefrom. Hemi- 
plegia with lower facial palsy indicates a lesion in the pos- 
terior half of the internal capsule. Hemiplegia with an 
opposite (crossed, alternating) ocular paralysis is due to a 
lesion in the crus. Hemiplegia with opposite facial palsy indi- 
cates a lesion of the pons. Hemiplegia with difficulty in 
articulation and deglutition (not aphasia) is due to a lesion of 
the medulla. Diplegia is the result of a bilateral or symmet- 
rical cerebral lesion, and occurs principally in children. 

As a rule, hemiplegia is the result of cerebral hemorrhage, 
thrombosis, or embolism; it is sudden in onset, but is often 
preceded by arterio-sclerosis, and it is followed by softening. 
Uremia occasions a transient hemiplegia, hysteria a functional 
variety; and a gradual, progressive hemiplegia may be due to 
a brain tumor or an island of sclerosis. 

Spastic paraplegia, if the sphincters are involved or the re- 
flexes exaggerated, is certainly due to a lesion of the cord. It 
may be due to spinal meningitis, Pott's disease, hereditary 
ataxic paraplegia, lateral sclerosis, disseminated sclerosis, 
chronic myelitis, transverse myelitis, syphilis, or the spastic 
cerebral paralysis of children. Flaccid paraplegia may be due 
to spinal disease (Friedreich's ataxia, acute poliomyelitis, 
intra-spinal hemorrhage, tumor, or tuberculosis) or to neuritis. 

Monoplegia, if cerebral, is almost invariably cortical or 
slightly sub-cortical; it may be due to hemorrhage, embolism, 
tumor, etc., and the paralysis is of cerebral type, i. e., spastic, 
non-atrophic. If spinal, a monoplegia is usually due to polio- 
myelitis or unilateral myelitis. More often the cause is peri- 
pheral, i. e., neuritis, and is distinguished by its limitation to 
the muscles supplied by a certain nerve. When neuritis is 



DISEASES OF THE NERVOUS SYSTEM. 381 

widespread, however, it may be difficult or impossible, because 
it is a disease of the lower neuron, to exclude a lesion of the 
anterior horn of the cord. 

2. The state of the muscular nutrition. Pinch the muscles and 
note whether they are firm or wasted and flabby. This is a 
rough test, but if only one limb is affected, comparison with 
the other renders it effective. 

A more delicate test of the muscular nutrition is afforded by 
investigation as to their electric irritability. For this purpose it 
it necessary to have a galvanic and a faradic battery, together 
with a rheostat, a milliamperemeter, and a switch for changing 
the direction of the galvanic current. Begin with the faradic 
current. The examiner should first test the strength of the 
latter upon his own wrist, in order to be sure that it is very 
weak at the start. Place a large (indifferent) electrode be- 
tween the shoulders or on the chest or abdomen, and apply a 
small (normal) electrode upon the nerve or motor points of 
the muscle to be examined. Note the minimum intensity of 
current (indicated by the distance to which the inner and 
outer coils overlap) which produces contraction at each point, 
and compare it with the effects of a similar current upon the 
corresponding point on the other side of the body. 

Then use the galvanic current. Place the electrodes in ex- 
actly the same positions as before, and arrange the switch so 
that the small electrode becomes the negative pole or cathode. 
Turn on the current and let it run for a moment; and open 
and close the circuit in this way several times, while slightly 
increasing or decreasing its strength, until the minimum force 
which will cause a muscular contraction at the instant of clos- 
ing the circuit has been ascertained. . This represents the 
cathodal closing contraction (CaCC). Note the strength of 
current indicated on the milliamperemeter. 

Reverse the direction of the current, thus making the small 
electrode the positive pole or anode. Repeat the same tests, 
thus ascertaining the anodal closing contracture (AnCC). 
By using the same strength of current in each case, determine 
whether CaCC is stronger or weaker than AnCC. The char- 



382 DISEASES OF THE NERVOUS SYSTEM. 

acter of the muscular contraction is also of great significance, 
e. g. } quick and sharp, slow or sluggish, or continuous and 
tetanic. 

Exceptionally it is necessary to make similar tests with the 
opening of the cathodal circuit (CaOC) and of the anodal 
(AnOC). 

The Reaction to Electrical Stimulation. — In health a sharp 
contraction follows closure of the faradic current and con- 
tinues as long as the passage of the latter. When the gal- 
vanic current is applied, contractions appear only at the open- 
ing and closing of the circuit. Normally, CaCC is the first to 
appear, and a decidedly strong current is necessary to induce 
AnCC. Still further increase of current is necessary to elicit 
AnOC and CaOC. Moreover, in health the muscular con- 
tractions are sharp and abrupt. 

/;/ disease these reactions to electrical stimulation may 
undergo either quantitative or qualitative alterations. Quan- 
titative alterations are present when a given current produces 
greater or less contraction than it would were the nerves and 
muscles normal. Qualitative alterations are indicated by a 
change in the character of the contraction, the latter becom- 
ing sluggish, or the cathodal closing contraction being more 
difficult to elicit than the anodal contractions. In their typical 
form these alterations constitute the reaction of degeneration. This 
is indicated as follows: 

1. With the faradic current — no response. 

2. With the galvanic current — sluggish response (extremely 
significant), and a response to the positive pole which is as 
good or even better than that to the negative pole. 

Significance of Altered Electrical Responses. — These 
changes are due to separation of the nerve and muscle from 
their nutritive centre, the cell body. In other words, a lesion 
of the lower neuron is present. If the reaction of degeneration 
is obtained, the examiner can exclude cerebral disease, func- 
tional paralysis, and muscular dystrophy; and he can posi- 
tively assert that some disease of the lower neuron (anterior 
cornua and roots or peripheral nerves) is present. 



DISEASES OF THE NERVOUS SYSTEM. 383 

3. Muscular co-ordination. The harmonious co-operative action 
of groups of muscles is necessary to perfect movement or 
station, and through the disturbance of this harmony certain 
acts become difficult. Inco-ordination {ataxia) may be due 
to absence of vision, to disturbance of cutaneous sensibility, 
or to loss of the muscular, articular, and tendinous senses 
whereby the sensorium is cognizant of the position of the vari- 
ous limbs and parts of the body. 

Tests. — Upper limbs. Bandage the eyes and then ask the 
patient to touch the tip of his nose first with one forefinger, 
then with the other; or require him to bring the tips of his two 
forefingers together. If he is able to do these things, no inco- 
ordination is present. 

Lower limbs. Request the patient to walk along a straight 
line, such as a crack in the floor; or if he is lying in bed, ask 
him to touch the dorsum of one foot with the great toe of the 
other. Inability to do this constitutes motor ataxia. 

Require the patient to stand with his heels together and his 
eyes closed, and note whether he sways markedly. If he does, 
static ataxia (Romberg's symptom) is present. 

Cerebellar ataxia, due to disturbance of equilibration by 
cerebellar disease, is characterized by a reeling, drunken gait. 
If the patient is in bed, he can successfully co-ordinate his 
lower limbs, imitating, with his foot, movements (circles in the 
air, etc.) made by the examiner's hand, touching stated points 
with his great toe, etc. In addition, the arms do not become 
ataxic. 

4. Abnormal muscular movements. Examination of the motor 
functions may reveal an abnormal degree of muscular con- 
traction, i. e., spasm. If this spasm is painful, it is called a 
cramp. If it consists of a more or less continuous contraction, 
the spasm is tonic. A paralyzed muscle which is constantly in 
a state of tonic spasm is said to be spastic, and this muscular 
contraction if long-continued leads to a permanent contracture* 

On the other hand, there may be alternate contraction and 
relaxation of the muscle {clonic spasm), and if this action 



384 DISEASES OF THE NERVOUS SYSTEM. 

involves a majority of the muscles, a "fit" or convulsion is 
said to be present. Both clonic and tonic spasms are seen in 
the convulsions of children and those of epilepsy, uremia and 
hysteria. Pure tonic spasms are present in tetanus and tetany. 

Tremor is the simplest form of clonic spasm. It consists of 
a trembling movement, especially of the extremities, and 
sometimes affects the eye ball {nystagmus}. According to 
the amplitude of the movements a tremor is said to be fine or 
coarse, and it may be slow or rapid. The movements may be 
present while the muscle is at rest {passive tremor), or it may 
begin or increase when voluntary movement is attempted 
{intention tremor). The tremor may involve the entire body or 
a single limb or a group of muscles. Exceptionally, only a 
few muscle fibres are affected {fibrillation), and this fibrillary 
spasm may be seen as a few irregular twitchings under the 
skin (progressive muscular atrophy, neurasthenia). 

Tests. — Let the patient stretch out his arms with the fingers 
extended and as wide apart as possible. If the tremor cannot 
then be seen, touch the patient's fingers with the hand and a 
thrill may be felt. Tremor of the tongue or face is best ex- 
hibited when the patient closes his eyes and protrudes his 
tongue vigorously for a few moments. Intention tremor is 
brought out by having the patient attempt some delicate co- 
ordinate movement, such as carrying a cup to his lips. 

Tremor may be merely a sign of excitement in nervous 
people. A persistent tremor is characteristic of certain dis- 
eases, notably exophthalmic goitre, disseminated sclerosis, 
and paralysis agitans; and it occurs with less regularity in 
senility and in alcoholic and other intoxications. 

Athetosis. — Athetoid movements consist of continuous, un- 
ceasing twisting motions of the fingers and hands, sometimes 
the toes and feet. They are occasionally seen in hemiplegics. 

Convulsions may be general, involving the entire body, or 
local, confined to a limited area, such as the face or one ex- 
tremity. A local convulsion which gradually extends to the 
adjacent muscles, with slight or tardy loss of consciousness, is 



DISEASES OF THE NERVOUS SYSTEM. 385 

called Jacksonian, and usually indicates irritation of a partic- 
ular point in the cerebral cortex, the exact location of which 
may be judged by the initial spasm {signal symptom}. 

Choreic movements consist of abrupt, jerking motions, invol- 
untary and objectless, of certain muscle-groups. They are 
seen not only in chorea but in a number of other affections 
(e. g., Huntingdon's chorea, habit chorea), and are sometimes 
induced by the intense toxemia of an acute infectious disease. 



IV. SENSORY FUNCTIONS. 

The investigation of the sensory functions of a patient 
should include, in addition to sight, hearing, smell, and taste 
(see Cranial Nerve Functions), tests for common sensibility 
(touch and pressure), and the pain, temperature, and muscu- 
lar senses. For this examination the patient should be blind- 
folded and instructed to maintain silence, signifying by mono- 
syllables his responses to the tests applied. Note not only the 
correctness but the promptness of his replies. 

1. Common sensibility, (a) Tactile sense. For delicate testing 
the esthesiometer, which is virtually a pair of compasses with 
blunt points, may be used. For practical purposes, however, 
it is enough to draw the tip of the finger, the end of a pencil, 
or a bit of cotton lightly across the patient's skin, asking him 
to say "now" when he feels it. Compare corresponding 
points on the opposite sides of the body, and occasionally 
omit the touch, in order to prevent unthinking responses from 
the patient. Ask him also to point out the exact spot touched; 
if he errs by more than two inches, slight anesthesia is 
present. 

Tactile sensibility may be abolished {anesthesia) as the 
result of interruption to the sensory paths at any point be- 
tween the periphery and the brain. This may be in the 
cerebrum (especially lesions of the sensory portion of the in- 
ternal capsule), the posterior nerve roots (tabes dorsalis), 
or the peripheral nerves (neuritis). Anesthesia, often of 
25 



386 DISEASES OF THE NERVOUS SYSTEM. 

peculiar distribution, constitutes one of the stigmata of hys- 
teria. Increased tactile sensibility {hyperesthesia), as a result 
of which a mere touch may be painful, is often present over 
hysterogenic zones. It also occurs in connection with menin- 
gitis, neuritis, and certain other diseases. 

{b) Pressure sense. The sense of pressure may be tested by 
supporting the part to be examined upon a bed or other sup- 
port, and placing upon it objects similar in size, but differing 
in weight {e. g., coins), and asking the patient to say which is 
the heavier. Loss of the pressure sense, tactile sensation re- 
maining, may be observed in tabes dorsalis. 

2. Pain sense. The point of a pen or a sharpened pencil may 
be employed to test the acuteness of the pain sense, the ex- 
aminer touching the symmetrical parts. It may be absent 
{analgesia) in syringomyelia, Morvan's disease, and hysteria; 
it is usually exaggerated {hyperalgesia) in association with 
hyperesthesia. 

3. Temperature sense. Fill two test tubes, one with hot and 
the other with cold water. Touch the skin with each in turn, 
asking the patient whether it feels hot or cold, and note 
whether he answers correctly. The temperature sense is lost 
in syringomyelia, and to a lesser degree in tabes dorsalis and 
diseases of the medulla. 

4. The muscular sense, with which are included the articular 
and tendinous senses, may be tested in two ways, {a) Weights, 
such as were employed in testing the pressure sense, are 
placed over the part to be tested, which in this case should be 
without support. The patient is requested to say which weight 
is the heavier, {b) The examiner moves one of the patient's 
extremities, flexing or extending it, and requests the patient to 
move the opposite limb in a similar fashion. Or, one limb may 
be placed in a certain posture and the patient asked to describe 
it. Impairment or loss of the muscular sense distinguishes 
ordinary from cerebellar ataxia; it is associated with some 
varieties of cerebral diseases and with tabes dorsalis. 

Abnormal sensations {paresthesia) may be present but require 



DISEASES OF THE NERVOUS SYSTEM. 387 

no tests for their discovery. The commonest of them are 
numbness, "pins and needles," constriction, itching (pruritus), 
and a sensation as of insects crawling over the skin {formi- 
cation ) . 

Delayed sensation, the response of the patient being delayed far 
beyond the normal one-tenth of a second, may be associated 
Avith tabes dorsalis and various peripheral palsies. 



V. REFLEX FUNCTIONS. 

For the production of a reflex it is necessary for a stimulus 
to travel from the periphery along an afferent nerve to the 
motor cells in the cord or medulla, where it is transferred into 
an impulse which traverses an efferent (motor) nerve to cer- 
tain muscles and induces their involuntary contraction. Three 
classes of reflexes are recognized, viz., 

1. Superficial (cutaneous) reflexes. The following depend upon 
centres in the medulla : 

The Conjunctival Reflex. — Touch the conjunctiva and the eyelids close 
abruptly. The fifth is the afferent and the seventh the efferent nerve. 

Pupillary-Skin Reflex. — Stroke the skin of the chin or neck, and the 
pupils dilate. 

Palatal Reflex. — Touch the mucous membrane of the palate and the latter 
draws up. The ninth is the afferent and tenth and eleventh the efferent 
nerves. 

The more important reflexes dependent upon the spinal cord 
are as follows : 

Plantar. — Stroking the sole of the foot is followed by movements of the 
toes, foot, or leg. (Lower part of lumbar enlargement.) 

Gluteal. — Stroking the skin of the buttock is followed by contraction of 
the gluteal muscles. (Fourth and fifth lumbar segments. ) 

Cremasteric. — Stroking the skin at the upper and inner part of the thigh 
is followed by retraction of the testicle. (First and second lumbar segments.) 

Abdominal. — Stroking the abdominal wall downward from the costal 
margin in the nipple line causes contraction of the abdominal muscles. 
{ Eighth to twelfth dorsal segments. ) 

Epigastric. — Stroking the side of the chest downward from the nipple is 



388 DISEASES OF THE NERVOUS SYSTEM. 

followed by a retraction of the epigastrium on the same side. (Fourth to 
seventh dorsal segments. ) 

Scapular. — Stroking the skin in the inter-scapular region causes contrac- 
tion of the scapular muscles. (Fifth cervical to first dorsal segments.) 

The significance of a superficial reflex is practically limited 
to a demonstration of the integrity of the reflex arc (sensory 
nerve, spinal segment, motor nerve) upon which it depends. 

2. Deep (tendon) reflexes. — When a muscle is put upon the 
stretch and its tendon sharply struck, it contracts abruptly. 
The more important of the reflexes thus obtained are the fol- 
lowing: 

The Jaw Jerk. — Place a ruler on the lower incisor teeth, or 
the finger upon the chin, while the mouth is partially opened, 
and upon the ruler or finger deliver a sharp percussion stroke. 
The masseter and temporal muscles contract sharply, closing 
the jaw. (Motor nucleus of fifth nerve.) 

The Elbow or Triceps Jerk. — With the elbow flexed, the 
arm resting upon the examiner's hand or upon the back of a 
chair, and the forearm hanging limply downward at a right 
angle, tap just above the point of the elbow. The forearm 
performs a quick movement of extension. 

The Wrist Jerk. — With the hand hanging down as in wrist- 
drop, strike the extensor tendons near the wrist joint. The 
hand is suddenly extended, 

The Knee Jerk.— The knees may be crossed, the patient 
may sit on a chair or table high enough to keep his feet from 
the floor, or the examiner may support the leg by placing his 
hand or arm under the crook of the knee. The leg must hang 
loosely. Then strike a sharp blow on the tendon just above 
the patella. This should be followed by a sharp jerk of the 
leg and foot. If the latter does not occur, require the patient 
to hook his hands together and pull with all his strength 
("reinforcement"); under these circumstances the knee jerk 
can, in health, almost always be elicited. 

The Ankle Jerk. — Extend the patient's leg and grasp the 
foot, bending the latter upward so as to put the tendo achilles 



DISEASES OF THE NERVOUS SYSTEM. 389 

on the stretch. Strike the latter sharply, and notice the re- 
sulting contraction of the calf muscles. 

Ankle Clonus. — With the leg partially extended and the 
knee slightly bent, hold the heel on the left hand and with the 
right abruptly push up the front part of the foot toward the 
leg and press steadily. Under certain abnormal circumstances 
a rhythmic, clonic movement ensues, and is continued for 
some time. 

Significance of the Tendon Reflexes. — The deep reflexes of 
the upper extremity may be absent in health. The jaw jerk 
is always abnormal; the presence of it and the elbow and 
wrist jerk is strongly suggestive of central disease. The knee 
jerk is almost always present in health, but if any portion of 
its arc is interrupted, it is abolished. Loss of the knee jerks 
may, therefore, be due to disease of the peripheral nerves 
(neuritis), disease of the posterior roots or columns (tabes 
dorsalis, Friedreich's ataxia), disease of the anterior cornua 
(poliomyelitis, Landry's paralysis), or to myelitis affecting 
the second and third lumbar segments. Exaggeration of the 
knee jerk is due to lessened inhibition by the upper motor 
neuron, which may be due to paralysis of cerebral origin in- 
volving the pyramidal tracts, hereditary cerebellar ataxia, 
paralytic dementia, lateral sclerosis, amyotrophic lateral 
sclerosis, and myelitis. It may also be a symptom of hysteria, 
neurasthenia, arthritis deformans, tetanus, and strychnine- 
poisoning. 

The ankle jerk corresponds in significance to the knee jerk. 
Ankle clonus is present under the conditions which cause ex- 
aggeration of the knee jerk; it is particularly marked in dis- 
seminated and amyotrophic lateral sclerosis. 

3. Organic reflexes. Respiration, deglutition, micturition, and 
defecation depend upon complex muscular movements of 
reflex origin. Difficulty or pain in urination or defecation, and 
incontinence of either urine or feces may, therefore, possess 
great diagnostic significance. The centres controlling the 
rectum and bladder are situated in the fourth and fifth sacral 
segments. 



390 DISEASES OF THE NERVOUS SYSTEM. 



CEREBRAL LOCALIZATION. 

The following (Striimpell) affords a convenient summary of 
the main facts bearing on the localization of cerebral disease: 

(1) The most frequent cause of ordinary hemiplegia is a 
lesion of the pyramidal tract in the posterior limb of the in- 
ternal capsule. If the hemiplegia be persistent, then this tract 
is actually destroyed; if temporary, the tract has been func- 
tionally deranged for a time by focal disease in the neighbor- 
ing parts of the brain. 

(2) Monoplegic cerebral paralysis is usually due to affections 
of the cortex of the brain, that is, the central convolutions and 
the paracentral lobule. Monoplegia of the face and tongue is 
the result of lesions in the lower extremity of the anterior 
central convolution. Monoplegia of the arm is referable prin- 
cipally to some lesion of the middle third of the anterior cen- 
tral convolution. Monoplegia of the lower extremity implies 
some affection of the paracentral lobule. 

(3) Hemiplegia or monoplegia, if associated with epilepti- 
form convulsions affecting either one-half or one particular 
portion of the body, are almost always caused by cortical 
lesions. These same symptoms of motor irritation with ac- 
companying paralysis are likewise ascribable to some irritation 
of the above-mentioned regions of the cortex. 

(4) Hemiplegia with crossed paralysis of the oculomotor 
nerve indicates a lesion of the crura cerebri. 

(5) Hemiplegia with crossed facial paralysis implies, with an 
approach to certainty, that the lesion is situated in the pons. 

(6) Post-hemiplegic chorea seems to occur especially where 
there is focal disease in the neighborhood of the optic thala- 
mus or of the posterior part of the internal capsule. 

(7) Hemianesthesia seems to result principally from lesions 
of the most posterior portion of the internal capsule. 

(8) Hemiopia may be due to a lesion of the occipital lobe. 
Probably, also, a lesion of the posterior extremity of the in- 



DISEASES OF THE NERVOUS SYSTEM. 391 

ternal capsule may cause it, in which case it is usually asso- 
ciated with hemianesthesia. Finally, it may be produced by 
lesions of the posterior tubercle of the optic thalamus, or one 
of the anterior corpora quadrigemina, or of one of the optic 
tracts. 

(9) Genuine motor aphasia indicates disease of the 3d left 
frontal convolution. 

(10) Word-deafness seems to be due to disease of the 1st 
left temporal convolution. 

(11) Difficulty in articulation implies disease of the medulla, 
as does also dysphagia. 

(12) Staggering gait and vertigo are the most constant 
symptoms of cerebellar disease. Forced positions and forced 
movements are seen chiefly in connection with lesions of the 
crura cerebelli ad pontem. 

(13) Staggering gait and ocular paralysis are indicative of 
lesions of the corpora quadrigemina. 



DISEASES OF THE BRAIN AND ITS MEMBRANES. 
PACHYMENINGITIS. 

Inflammation of the dura mater may affect its outer surface 
{pachymeningitis externa) or its inner surface {pachymeningitis 
interna). 

Pachymeningitis externa is due to infection spreading from ad- 
jacent structures ^fracture of the cranium with sepsis, osteitis, 
necrosis, neoplasms, and suppurative middle ear disease). 
The dura becomes thickened, with adhesion to the inner sur- 
face of the cranium, and sinus-thrombosis or septicemia may 
ensue. Treatment should be directed to the primary condi- 
tion. 

Pachymeningitis interna (pachymeningitis hemorrhagica, hema- 
toma of the dura mater) is a chronic inflammation of the in- 
ner surface of the dura attended by hemorrhagic extravasa- 
tions between its layers, the effused blood becoming organized 



392 DISEASES OF THE NERVOUS SYSTEM. 

into laminated new membranes. It is due to vascular degen- 
eration, the result of alcoholism, infectious diseases, and 
cachectic conditions; and it is a constant association of para- 
lytic dementia. The symptoms are vague until pressure pro- 
duces cerebral manifestations, such as pain in the head, intel- 
lectual failure, Jacksonian convulsions, apoplectiform seizures, 
transitory hemiplegias, and rarely vomiting. The duration of 
the disease is variable, but it tends to death. Diagnosis is ex- 
tremely difficult, but the occurrence of the symptoms enumer- 
ated in drunkards or paretics may suggest the disease. Treat- 
ment should as far as possible be directed to the casual 
condition. 

LEPTOMENINGITIS. 

Etiology. — Inflammation of the pia mater (acute cerebral 
meningitis, purulent meningitis) may result from lesions of 
neighboring structures (cranial fractures, and septic infections 
of the scalp, face, middle ear, orbit, nares, etc.), or from 
microbic infection through the vascular supply (pneumonia, 
rheumatic fever, and other infections; coryza). The epidemic 
cerebro-spinal variety, due to the diplococcus intracellularis, 
has been described elsewhere. 

Pathology.— The infective agents (pneumococci, streptococci, 
typhoid bacilli, staphylococci, etc. ) may set up a localized in- 
flammation by extension from an adjacent focus; but when the 
infection occurs through the blood, the meningitis is general- 
ized, though most intense over the vertex. The arteries are 
engorged, and the membrane is roughened and more or less 
covered with a purulent exudate; the ventricles are dilated 
with the increased fluid, and the cerebral cortex is edematous, 
infiltrated with pus, and adherent to the pia. 

Symptoms. — The disease may be preceded by several days of 
malaise, feverishness and slight headache. A rigor may ac- 
company the onset, and four cardinal symptoms develop 
almost immediately, viz., 

1. Fever. While constant, this is rarely high (100-103°). 



DISEASES OF THE NERVOUS SYSTEM. 393 

2. Headache. This is violent and subject to paroxysmal 
exacerbations. Even when comatose the patient, by holding 
the head in the hands, by groans, and by facial expression, 
indicates its continued presence. 

3. Delirium. This is usually of a low type, but occasion- 
ally it is wild and maniacal. 

4. Vomiting. This is projectile in character and unaccom- 
panied by nausea. 

Associated with these symptoms there may be muscular 
rigidity, which in the neck is associated with retraction, and 
convulsions, particularly in children. Sooner or later the 
cranial nerves become involved, and as a result there may be 
photophobia, neuro-retinitis, strabismus, myosis, mydriasis, or 
immobile pupils, and deafness. Cutaneous hyperesthesia is 
present over the trunk and limbs, and if the finger nail be 
drawn across the skin of the abdomen, it is followed slowly by 
a red streak that persists for some minutes (tache cerebrale). 
The pulse may be full and active early in the attack, but later 
it is sluggish and slow (60-40), thus showing disassociation 
with the temperature. The bowels are constipated and the 
abdomen "scow-shaped." 

Course. — The disease may end fatally within twenty-four 
hours, or it may extend over several weeks. In the average 
case a week of active symptoms merges into a state of de- 
pression, with deepening coma and finally death from heart 
failure or bulbar involvement. 

Chronic Leptomeningitis may be a sequence of the acute va- 
riety, or it may be due to alcoholism, syphilis, or sunstroke. 
Clinically, except in the syphilitic form, its manifestations are 
so obscure as to render diagnosis impossible. 

Diagnosis. — In the presence of causal conditions, the appear- 
ance of the four cardinal symptoms mentioned will justify a 
tentative diagnosis of meningitis. Uremia should be excluded 
by careful urinalysis. 

Prognosis. — The mortality varies from 30 to 60 per cent., and 
even should recovery take place, permanent brain injury 



394 DISEASES OF THE NERVOUS SYSTEM. 

is apt to result. In no case can the outcome be foretold by 
the symptoms; the mildest attack may end fatally, the worst 
recover. 

Treatment. — Remove, if possible, the infective focus; render 
aseptic any cavity, cranial, optic, nasal, pharyngeal, intestinal, 
or pelvic, the contents of which justify suspicion. With 
this in view it is wise to empty the bowels by enemata or 
cathartics. Of medicines, aconite may be indicated by the 
early febrile symptoms, arnica by a history of traumatism, 
and belladonna by violent headache and delirium. The de- 
velopment of effusion is accompanied by symptoms which 
suggest the administration of bryonia. The convulsive phe- 
nomena may be met by the use of cuprum or cicuta. Among 
remedies less frequently useful are apis, gelseminm, glonoin, 
lielleborns, mercurius, cenanthe crocata, sulphur, and zinc. 

HYDROCEPHALUS. 

Etiology. — Increase of the quantity of cerebro-spinal fluid may 
occur within the ventricles {internal hydrocephalus) or in the 
sub-dural spaces {external hydroceplialus). It may be acute 
or chronic, congenital or acquired; but in a vast majority of 
cases it appears at birth or within the first six months of life. 
The causes are obscure, although parental syphilis and alcol- 
hoism are important factors, and meningitis, traumatic or 
otherwise, may induce it. 

Pathology. — In the majority of cases occurring before the 
cranial bones are united the head becomes greatly enlarged, 
the bones are thin and without diploe, and the sutures are open. 
The lateral ventricles are often enormously distended, and in 
half the cases the ventricular aqueducts are obliterated, the 
third and fourth ventricles thereby escaping. The contained 
fluid is colorless, of low specific gravity, and resembles other 
serous effusions. The convolutions and often the basal ganglia 
are compressed and flattened. Should the disease develop 
after cranial solidification has taken place, the head does not 
enlarge and the amount of fluid is less, but the pressure upon 
the cerebrum is consequently greater. 



DISEASES OF THE NERVOUS SYSTEM. 395 

Symptoms. — Hydrocephalus may render birth difficult and even 
necessitate the use of the perforator. As a rule, however, it 
is not noticed until the rapid enlargement of the head during 
the first year of life attracts attention. The outline of the 
skull is globular, and it appears to overhang the face, which is 
not similarly enlarged. The internal pressure is manifested 
in bulging fontanelles and open sutures, and the superficial 
veins of the scalp are distended. 

The child is inactive, often peevish and restless, and fre- 
quently repeats a distressed cry. It raises its head with diffi- 
culty or not at all. If death does not soon occur from ex- 
haustion, convulsions, or coma, retarded growth usually mani- 
fests itself in a dwarfish body and a mental development which 
is defective in varying degrees. Optic atrophy and blindness, 
nystagmus, strabismus, and spasticity of the lower limbs are 
frequently associated with the other symptoms. 

Diagnosis. — The enlarged globular head usually affords a 
diagnosis. In the only similar condition, rachitis, the head is 
not round, but square, with a bulging forehead, and rickety 
conditions may be detected in the long bones and at the costal 
extremities. In the absence of cranial enlargement the dis- 
ease can be discovered only post mortem. 

Hj/drocep/ia/oid (hydrencephailoid, spurious hydrocephalus), 
is a term applied by Marshall Hall to a condition supervening 
upon infantile diarrheas in which the patient becomes semi- 
comatose, with fingers clutched, head retracted, and respira- 
tion irregular. The condition has been attributed to cerebral 
anemia, followed by venous hyperemia and consequent effu- 
sion. It is more probably the result of aute-intoxication. It 
bears no relation whatever to true hydrocephalus. 

Prognosis. — In a vast majority of cases death occurs within a 
year. A few patients live for several years, but their life is 
much shortened and their mentality is very poor. In rare 
cases the disease becomes stationary, and a fair degree of 
mental and physical development and a long life become 
possible. 



396 DISEASES OF THE NERVOUS SYSTEM. 

Treatment. — This is very unsatisfactory. When the process 
is active, cold may be applied to the head. Some success has 
attended exposure of the child's head to the sun, beginning 
with twenty minutes each day and increasing to thirty or 
forty. Strapping the head with adhesive plaster has been 
tried; but it causes intolerable pain and only serves to increase 
the intracranial pressure. Repeated tapping through the fon- 
tanelles or by lumbar puncture has in a few cases been at- 
tended with apparent success; only a small amount of fluid 
should be withdrawn at one time, and strict antisepsis is 
necessary. Attempts at permanent drainage have almost in- 
variably been followed by death. A method recently devised 
consists of the introduction of drainage tubes through a drill 
opening above and back of the ear; union is then secured 
between the covering scalp-flaps and in the cavity thus formed 
the fluid is allowed to accumulate and reabsorb. 

Medicines should be prescribed according to the underlying 
constitutional conditions rather than mere symptoms; the more 
important are the calcareas, arsenic, baryta carb., kali iod., 
lycopodium, merciirius, and sulphur. 

CEREBRAL ANEMIA. 

Etiology. — Cerebral anemia is invariably secondary. It is 
often associated with general anemia or cachexia; it may be 
due to mechanical causes, such as an insufficient heart or oc- 
clusion of a carotid by ligation or atheroma; it results from 
emotional excitement, such as pain or shock; and it can be 
induced by various poisons, such as tobacco, ergot, chloro- 
form, and the bromides. 

Symptoms. — Cerebral anemia may be acute, as in an ordinary 
fainting fit following great loss of blood. Under such circum- 
stances the patient becomes giddy, hears noises in the ears, 
everything grows dark before his eyes, and he loses conscious- 
ness more or less completely. 

In the chronic cerebral anemia attendant upon general 
anemia, etc., the patient suffers with dull headaches and a 



DISEASES OF THE NERVOUS SYSTEM. 397 

sense of heaviness or constriction about the head. Vertigo, 
tinnitus, and muscse volitantes may be noted, especially when 
he rises suddenly. The mental condition is altered; the pa- 
tient is inclined to be irritable and peevish, and he is physically 
inactive. 

Diagnosis and treatment should be directed to the underlying- 
cause. 

CEREBRAL HYPEREMIA. 

Etiology. — Acute congestion of the brain occurs normally 
under the influence of great excitement or unusual mental or 
physical exertion. It may be caused by certain drugs (nitrites, 
alcohol), certain infectious diseases (typhoid, typhus, etc.), or 
by sunstroke. Menstrual suppression, or the menopause, may 
induce cerebral hyperemia; and overactivity of a hypertrophied 
heart, or the vascular "storms" of the gouty, may underlie 
its occurrence. 

A chronic cerebral congestion, passive in character, may be 
the result of heart lesions or other conditions impeding the 
venous return, or it may be associated with chronic disease of 
the brain itself. 

Symptoms. — Acute cerebral congestion, if marked, causes a 
throbbing headache, blurred vision, photophobia, vertigo, 
tinnitus, and frightful dreams during sleep. Delirium or con- 
vulsions may supervene, or even an apoplectiform attack may 
be induced. Chronic hyperemia is accompanied by a sense 
of fulness, a dull frontal headache, and various mental symp- 
toms. 

Diagnosis.- — The sense of fulness in the head associated with 
flushed face, throbbing arteries, and aggravation when the 
head is lowered, is usually sufficient to distinguish cerebral 
congestion. It is necessary, however, to discover its cause, 
and to that treatment must be directed. 



398 DISEASES OF THE NERVOUS SYSTEM. 



INTRACRANIAL HEMORRHAGE. 

(Cerebral Apoplexy.) 

Etiology. — Hemorrhage into the substance of the brain is 
the direct result of the coincidence of two factors, viz., 

1. High arterial tension. A strong, forcible heart driving 
the blood into inelastic arteries produces high tension within 
the cerebral arteries. The hemorrhage may, therefore, be 
directly induced by emotional excitement, over-exertion, 
coughing, sneezing, vomiting, or chilling of the surface of the 
body, all of which tend to force more blood into the cerebral 
circulation. 

2. Lessened resistance of the arterial walls. Arterial dis- 
ease, inflammatory or degenerative, may be associated with 
gout, syphilis, alcoholism, plumbism, or chronic nephritis. 
This arterial condition is usually present in the aged, and in 
childhood the arteries are naturally weak; consequently it is 
in early life and advanced age that intracranial hemorrhage is 
common. In some cases there appears to be a hereditary 
tendency to cerebral hemorrhage. 

Pathology. — All parts of the brain are subject to arterial dis- 
ease and in consequence thereof to hemorrhage; but by far the 
most frequent site of the latter is the area about the lenticulos- 
triate branches which arise from the trunk of the middle cere- 
bral artery and supply the basal ganglia and the internal and 
external capsule. Next in order of frequency are the centrum 
ovale, cortex, cerebellum, pons, medulla, crura, and corpus cal- 
losum. Usually by the rupture of a miliary aneurism in the 
vessel wall, blood is extravasated, and the latter separates or 
breaks through the tissues adjacent to the site of the hemorr- 
hage. There later it undergoes clotting, the serum is absorbed, 
and the remaining ocherous mass, consisting of blood-crystals, 
pigment and fatty detritus, may become encysted and even 
cicatrized. The motor tracts intercepted by the lesion under- 
go a degeneration which extends down the entire length of 



DISEASES OF THE NERVOUS SYSTEM. 399 

the neuron, and involves the lateral tracts of the cord, espe- 
cially on the side opposite the lesion. 

Symptoms. — Rarely momentary confusion or vertigo precedes 
the attack, but as a rule the onset is abrupt— a "stroke." 
Consciousness is almost instantly abolished, and the patient, 
if upright, falls. At first the face is pale, the pupils con- 
tracted, and muscular twitchings or even general convulsions 
may occur. In the "apoplectic" state which ensues the 
patient lies inert, unconscious, and his breathing may be slow, 
stertorous, or of the Cheyne-Stokes type. His face becomes 
congested, all forms of sensibility are abolished, and the 
sphincters are relaxed. It is often difficult to detect the pa- 
ralysis at this time, but already the patient tends to direct his 
face and eyes to the side of the brain that contains the hemor- 
rhage {conjugate deviation), the arm or leg of the paralyzed 
side, if lifted, falls limply, and whatever slight movements the 
patient makes are restricted to the sound side. 

This coma may deepen into death, or it may pass off. In 
the latter case, a period of torpor ensues, from which the 
patient can temporarily be aroused by painful stimulation, 
such as pinching. Then he begins to hear loud voice sounds, 
and finally by facial expression and attempts at speech he 
indicates his partial return to consciousness. For some hours 
he is still inclined, if undisturbed, to relapse into stertorous 
sleep; but finally consciousness becomes completely restored. 

The Hemiplegia state which follows intracranial hemor- 
rhage may also, it must be remembered, result from traumatic 
lesions of brain and cord, from meningeal lesions (hemor- 
rhage, inflammation, syphilis and tuberculosis), from cerebral 
lesions (softening, tumors, abscesses, and sclerosis), and from 
cerebro-spinal lesions (locomotor ataxia, disseminated scler- 
osis, and paretic dementia). In cases of hemiplegia due to 
intracranial hemorrhage, if death does not occur within three 
weeks after the onset, the hemiplegia begins to improve 
and continues to do so steadily for several months. The 
exact degree of paralysis that will persist cannot, how- 
ever, be foretold; in some cases it remains extreme, in 



400 DISEASES OF THE NERVOUS SYSTEM. 

others it becomes very slight. At first the reflexes are abol- 
ished and the muscles limp, but gradually, as the result of de- 
generation extending down the lateral tracts, the reflexes return 
and become exaggerated, the paralyzed limb becomes spastic, 
and clonus develops. In from one to four months after the 
attack the period of late contractures is established, the limbs, 
as a result, becoming rigid in certain characteristic deformities. 
Post-hemiplegic motor phenomena, such as rhythmical tremors 
or irregular movements, choreiform or athetoid, may now 
appear. 

Diagnosis. — During the period of unconsciousness it is neces- 
sary to exclude syncope, poisoning, and alcoholic intoxication. 
If hemiplegia can be detected, nothing more is necessary; but 
if it cannot, the pale face and weak pulse of syncope, the con- 
tracted pupils of opium-poisoning, and the odor of alcohol 
may aid in distinguishing those conditions. It must not be 
forgotten, however, that frequently the patient has been given 
alcoholic stimulants or that intracranial hemorrhage may de- 
velop after the patient has taken alcohol. Uremia may be yet 
more difficult to detect, since cerebral hemorrhage is so fre- 
quently associated with chronic interstitial nephritis. Convul- 
sive rather than paralytic features usually distinguish such 
cases, however. Meningeal hemorrhage presents similar symp- 
toms, but it usually follows injury after a short interval, and is 
accompanied by cranial nerve irritation and bilateral convul- 
sions. An attack of Jaeksonian epilepsy may be due to cortical 
hemorrhage, but such attacks are common to all lesions of the 
cerebral motor area. Rarely hysteria produces a very exact 
imitation of intracranial hemorrhage, but the age of the 
patient and her history are usually significant. Cerebellar 
hemorrhage is sudden in onset, the patient falls, vomits, and 
is extremely dizzy, while the attack occasions much less dis- 
turbance of mind and consciousness than does cerebral hemor- 
rhage. 

It is extremely important to both prognosis and treatment 
that if possible a distinction be made between hemorrhage, 
the extravasated blood of which may become encapsulated, 



DISEASES OF THE NERVOUS SYSTEM. 



401 



and thrombosis, which is a prelude to softening. The follow- 
ing table will aid in this differentiation: 



Hemorrhage. 

Frequent before third year and be- 
tween fortieth and sixtieth. 
Attended by high arterial tension. 
Incited by emotions, effort, or shock. 



No prodromes. 

Sudden, complete stroke. 

Coma complete. 

Face congested. 

Respiration stertorous. 

Pulse slow, full, bounding. 

Hemiplegia, complete at onset. 

Rapid improvement in motion fol- 
lows. 

Anesthesia transitory. 

Persistent aphasia unusual. 

Post-hemiplegic athetosis and chorea 
common. 

Post-hemiplegic convulsions rare. 



Thrombosis. 

Frequent in young adults and in the 
very old. 

Low arterial tension. 

Rarely excitement or effort, except 
in embolism; rather favored by 
sleep. 

Prodromes usual. 

Less complete. 

Coma slight or wanting. 

Face pale. 

Respiration undisturbed. 

Pulse weak, often frequent. 

Often monoplegic, but inclined to ex- 
tend. 

Slow improvement, or even exten- 
sion of the paralysis. 

Persistent paresthesia. 

Persistent aphasia. 

Uncommon. 

Common. 



Prognosis. — Intracranial hemorrhage is the result of ad- 
vanced arterial disease, and hence recurrence is possible. 
Two-thirds of the patients survive the first attack, but very 
few a second or third. Prolongation of the coma for a longer 
period than three days, or the appearance of Cheyne-Stokes 
respiration, convulsions, pneumonia, or bed sores, presages a 
fatal termination. 

The paralysis, if unimproved within a week, is likely to be 
permanent. Should improvement begin it is apt to be pro- 
gressive for the first three months, but after that period only 
slight further change is to be anticipated. 

Treatment. — If the diagnosis of intracranial hemorrhage is 
positive, active measures to reduce arterial tension may be 
26 



402 DISEASES OF THE NERVOUS SYSTEM. 

adopted: the head raised, an ice-cap placed upon it, and heat 
applied to the lower extremities. Pressure may be made upon 
both carotids; or "bleeding into the veins," by applying a 
tourniquet to prevent the return flow from the lower ex- 
tremities, may be tried. If there is much arterial excitement, 
aconite or veratrum viride should be given; if cerebral con- 
gestion is prominent, belladonna; and if nephritis coexists, 
glonoin. Marked venous congestion and profound stupor will 
suggest the administration of opium. 

As a rule the hemorrhage reaches its maximum within four 
hours, and thereafter the object of treatment is largely to pre- 
vent a recurrence. For this purpose quiet, warmth, cleanli- 
ness, and a liquid diet are essential. The bladder should be 
emptied, and care taken that the inhalation of food or mucus 
does not set up an aspiration-pneumonia. When coma has 
passed away, gentle massage and mild faradism may be ap- 
plied daily to the paralyzed muscles. Contractures should be 
antagonized by encouraging voluntary control, and for this 
purpose it is well to have the two sides of the body perform 
movements simultaneously. Causticum, baryta carb. and sul- 
phur are recommended as remedies promoting absorption of 
the clot. 

CEREBRAL SOFTENING. 

(Embolism; Thrombosis.) 

Etiology. — Acute softening of the brain follows the plugging 
of a cerebral blood vessel by — 

1. An embo.us, generally consisting of small, soft particles 
of fibrin which have been detached by the blood current from 
the valves of the heart. Rarely, an embolus may originate in 
inflammatory or degenerative lesions affecting the vascular 
system outside of the heart, but as a rule it arises from endo- 
carditis complicating an infectious disease. It is, therefore, 
most common in the young. 

2. A thrombus, either (a) deposited upon an embolus, or 
(b) developing in situ upon the inner coat of a vessel. In the 



DISEASES OF THE NERVOUS SYSTEM. 403 

latter case the vessel-wall is usually degenerated (arterio- 
sclerosis, syphilis), and in addition the blood current is slowed, 
and consequently the process of coagulation favored, by weak- 
ness of the heart's action. It is, therefore, most frequent in 
the aged. 

Pathology. — Because of the deficient anastomosis of the cere- 
bral circulation, occlusion of a vessel cuts off the blood supply 
from a certain territory. In twenty-four hours this area begins 
to soften and subsequently it is absorbed, leaving a cicatrix or 
cyst. If the occlusion is due to an embolus containing in- 
fective organisms, local encephalitis and an abscess may result. 

An embolus usually enters the brain by one of the carotids, 
especially the left, and traverses the internal carotid to the 
left middle cerebral in the fissure of Sylvius; rarely it enters 
by the vertebral and its posterior cerebral branch. A throm- 
bus affects the middle cerebral and basilar most frequently; it 
may, however, plug the posterior cerebral, the vertebral, the 
branches of the circle of Willis, and the basilar at its bifurca- 
tion. Occasionally it may involve the sinuses. 

Symptoms. — Embolism is rarely preceded by prodromes. As a 
rule, there is a sudden onset of hemiplegia, associated with 
temporary vertigo, confusion, or loss of consciousness, but little 
or no coma. 

Thrombosis is usually preceded by vertigo, transient aphasia 
or hemiplegia, numbness of the hand and foot, and drowsi- 
ness; in syphilitic cases there may be headaches and cranial 
nerve palsies. The onset is often rather gradual, hemiplegia 
developing in the course of several hours and the patient in the 
meantime becoming comatose. In some cases, however, the 
onset is so abrupt that it is difficult to exclude hemorrhage. 

The acute softening of the brain tissue which ensues may 
kill within twenty-four hours, but generally the patient sur- 
vives for several weeks at least. After the acute stage has 
passed the patient develops the hemiplegic state described as 
the sequence of intracranial hemorrhage. 

Diagnosis. — The distinction between acute softening and 



404 DISEASES OF THE NERVOUS SYSTEM. 

hemorrhage has been considered in connection with the latter 
disease. Embolism may be distinguished from thrombosis 
by the age of the patient, the co-existence of heart disease, 
and the suddenness of the onset. 

Prognosis. — In embolism the danger of recurrence is much 
less than in thrombosis, and the mental condition is better. 
The prognosis for the hemiplegia, after the chronic stage has 
been reached, is about the same in embolism, thrombosis, 
and hemorrhage. 

Treatment.— Place the patient at rest in bed with the head 
raised. Attend to the activity of the heart, kidneys, and 
bowels. Weakness of the heart may justify the administra- 
tion of alcoholics or of digitalis, preferably in conjunction 
with glonoin. Syphilitic cases should receive mercury and the 
iodides. The hemiplegia should be treated in the same man- 
ner as that due to hemorrhage. 

INTRACRANIAL TUMOR. 

Etiology. — The causes of intracranial tumors are as obscure 
as those of neoplasms elsewhere. Certain varieties (e. g., 
tubercles, gummata, echinococcus cysts) are readily explained. 
Heredity may play a part in the production of cancer, gumma, 
and tubercle; and traumatism may predispose in some cases. 
The tubercle is frequent in children; otherwise, adult males 
are most often afflicted. 

Pathology. — The most common form is the tyroma (tubercle), 
the encysted caseous masses of which are often multiple. Next 
in frequency is the gumma, not unlike the tubercle in appear- 
ance, but, unlike it, capable of retrogression. The sarcoma 
usually occurs as a single encapsulated neoplasm of rapid 
growth which can easily be enucleated. The glioma, a soft, 
reddish tumor arising from the neuroglia, is infiltrating and 
destructive in its tendency. It is frequently mixed with sar- 
coma {glio-sarcoma). The carcinoma, practically always 
secondary to a growth elsewhere, develops in the second half 
of life, and appears as an ill-defined nodular growth which is in- 



DISEASES OF THE NERVOUS SYSTEM. 405 

operable. Cysts are usually congenital {.porencephalies) , but are 
at times the result of hemorrhage or of the presence of para- 
sites (echinococcus, cysticercus). Aneurisms springing from 
any of the cerebral arteries may also give rise to the symp- 
toms of intracranial tumor. Other varieties (fibroma, neu- 
roma, psammoma, leproma, etc.) are rarely found in the 
brain. 

All brain tumors cause a certain amount of destruction in 
the surrounding tissue; if the meninges are reached, an inflam- 
matory thickening over the growth occurs; and should the re- 
turn circulation from the ventricles become obstructed, a 
condition of internal hydrocephalus is added. 

Symptoms. — The clinical picture varies according to the sit- 
uation of the tumor and the rapidity of its growth. As a 
rule, the symptoms are of two classes, viz., 

General symptoms due to increased intracranial pressure. 
The more important of these are — 

1. Headache. In a majority of cases this is early, per- 
sistent, and often intolerable. It is generally more intense 
the nearer the tumor is to the surface, probably through in- 
volvement of the meninges. Its location bears no necessary 
relation to that of the tumor. 

2. Insomnia. This may be the result of constant pain, but 
at times it occurs in the absence of the latter. 

3. Vomiting. Attacks of vomiting of cerebral type, i. e., 
without nausea or effort, are common, especially if the growth 
involves the cerebellum. 

4. Vertigo. Dizziness is particularly apt to accompany 
tumors in the cerebellar and frontal regions. 

5. Optic neuritis. Choked disc (papillitis) is present in 80 
per cent, of the cases of brain tumor, but it may also be the 
result of increased intracranial pressure due to other causes 
(e. g., abscess, meningitis). It is usually bilateral. 

6. Mental impairment. Mental vigor may be impaired early 
in the course of the disease, and in the later stages the patient 



406 DISEASES OF THE NERVOUS SYSTEM. 

is apt to sink into stupor or coma. In exceptional cases 
various psychoses (melancholia, mania, etc.) develop. 

Focal symptoms. Various localizing symptoms may occur. 
They consist of unilateral spasms confined to the face, to a 
limb, or to a segment of a limb; of aphasia, of monoplegias, 
of paresthesias, of hemianopia, or of cranial nerve disturb- 
ances. They may be associated with or initiate general con- 
vulsion? of epileptiform type. 

Diagnosis. — The existence of a tumor may be indicated by 
the symptoms enumerated; but it is then necessary to ascer- 
tain its location, and this is determined, if at all, by study of 
the focal symptoms in their relation to cerebral localization. 
The probable nature of the tumor may often be surmised after 
consideration of the patient's age, diathesis, and previous ill- 
nesses. In childhood, tubercle, glioma and sarcoma are the 
more common; in adults, the gumma may often be suspected; 
and in the aged, carcinoma. 

Meningitis is more rapid in its development than a brain 
tumor and the motor symptoms are usually bilateral. Uremic 
convulsions may assume the Jacksonian type, strongly sug- 
gesting a focal lesion, but repeated urinary examinations, and 
especially estimation of the amount of urea excreted, will 
serve to distinguish the disease. 

Prognosis. — In but seven per cent, of brain tumors is opera- 
tive interference practicable, and only the gumma is amenable 
to medical treatment. The general prognosis is, therefore, 
far from favorable. A large majority of cases end fatally 
within three years. 

Treatment. — Syphilitic cases should receive inunctions of mer- 
cury, and potassium iodide, often in enormous doses, should be 
given internally. If the tumor can be definitely localized, 
operative removal should be attempted. In the remaining 
cases only palliation is possible. 



DISEASES OF THE NERVOUS SYSTEM. 407 



ACUTE HEMORRHAGIC ENCEPHALITIS. 

Acute hemorrhagic encephalitis is a condition marked by 
the occurrence of multiple hemorrhagic, softened foci in the 
brain tissue. It is usually secondary to some infectious dis- 
ease, notably influenza. The symptoms are indefinite, often 
suggesting meningitis; they consist of headache, vomiting, 
convulsions, or localized palsies. Sluggish pupils and strabis- 
mus are common, and the patient is stuporous and inclined to 
sink into coma. The diagnosis is usually made post mortem, 
but it is probable that a fair proportion of the cases recover. 
The treatment is that of meningitis. 

PURULENT ENCEPHALITIS. 

(Brain Abscess.) 

Etiology. — Inflammation of the brain when caused by pyo- 
genic organisms eventuates in suppuration. The process may 
be diffuse or circumscribed. It is invariably secondary, espe- 
cially to — 

1. Suppurative middle ear diseases (40%). 

2. Head injury (25%). 

3. Pyemia (15%). 

4. Septic inflammations in the nose or pharynx, pulmonary 
tuberculosis, acute infectious diseases, etc., furnish most of the 
remaining cases. 

Pathology. — The pathway of invasion is frequently ob- 
scure, but usually the pyogenic organisms are conveyed to 
the brain through the arteries or venous channels. The 
frontal and temporal lobes are most frequently attacked. The 
size of the abscess may vary from that of a pea to that of an 
orange, and it may be single or multiple. In a majority of 
cases it is encysted. 

Symptoms. — The symptoms are often indefinite, but in many 
cases three stages are observed, viz., 



408 DISEASES OF THE NERVOUS SYSTEM. 

1. The stage of invasion. An intense and persistent head- 
ache, suggesting meningitis, is accompanied by a low, some- 
what septic, type of fever, and the occurrence of rigors or 
sweats occasionally serves to indicate the nature of the 
process. Mentally the patient is torpid, sometimes delirious. 
This condition may merge at once into the third stage, or it 
may be followed by — 

2. A stage of remission, due to encapsulation of the abscess. 
The early symptoms may entirely disappear, and for a variable 
time the patient appears perfectly well. Finally, however, 

3. The stage of pa7'alysis supervenes. Suddenly the abscess 
ruptures, infiltrating the capsule, invading the medulla, or 
tearing through the cortex. The symptoms are those of an 
apoplectic stroke, sometimes punctuated with focal convul- 
sions; and, as a rule, the patient dies within a few hours. If 
he should survive the stroke, hemiplegia develops and with it 
the headache, fever, and other symptoms of the early stage 
reappear, and death is seldom long delayed. 

Diagnosis. — The diagnosis rests largely upon a history of the 
onset of cerebral and septic symptoms following middle ear 
disease, head injury, or pyemia. Localizing symptoms are 
often entirely lacking. 

Prognosis. — Grave, and without operative interference, hope- 
less. 

Treatment.— Prophylaxis is most important; suppurations in 
the ear or nose and injuries about the head should, if possible, 
be made surgically clean. When the formation of a brain 
abscess is suspected, the aid of a surgeon should be invoked at 
once. 

SUPERIOR ACUTE POLIOENCEPHALITIS. 

(Nuclear Ophthalmoplegia.) 

Etiology. — Acute or subacute inflammation, often hemor- 
rhagic, of the central gray matter in the floor of the third 
ventricle and the aqueduct of Sylvius, involving the upper 
cranial nerve nuclei, may be due to: 



DISEASES OF THE NERVOUS SYSTEM. 409 

1. Toxic agents, notably alcohol, lead, carbon sulphide, and 
carbon dioxide. 

2. Infectious diseases, especially influenza, pneumonia, diph- 
theria, and syphilis. The lesion is closely related to that of 
poliomyelitis anterior, with which it is sometimes associated. 

Symptoms. — Premonitory symptoms, such as headache, di- 
plopia, and unsteady gait, or, in alcoholics, stupor or delirium, 
may precede the attack. As a rule, however, there is a rather 
sudden onset of paralysis of the upper cranial nerve nuclei on 
one or both sides. This is indicated by ptosis, internal con- 
vergence or fixedness of the eyeballs, and inactive pupils. In 
consequence the face becomes mask-like and expressionless. 
These symptoms vary according to the completeness with 
which the nuclei of the third, fourth, and sixth nerves are in- 
volved. Exceptionally they are associated with disturbances 
of gait, which vary from slight inco-ordination to a reeling 
suggestive of cerebellar ataxia. 

Prognosis.— The prognosis is very grave, especially in chil- 
dren. A majority die, but a few cases become stationary, and 
others merge into the chronic form. 

The treatment consists principally of rest and attempts to 
remove the infective or toxic cause. 



SUPERIOR CHRONIC POLIOENCEPHALITIS. 

Etiology. — This condition may be: 

1. A sequence of the acute form, or a result of the same toxic 
and infective causes. 

2. Secondary to locomotor ataxia, postero-lateral sclerosis, 
paralytic dementia, or disseminated sclerosis. 

Symptoms. — The symptoms are those of the acute form, but 
are much more gradual in onset. Beginning with a ptosis or 
squint, the other symptoms are added in the course of perhaps 
several years. Extension to the bulbar region or even to the 
cord mav ensue. 



410 DISEASES OF THE NERVOUS SYSTEM. 

The prognosis is unfavorable. Treatment may be directed to 
syphilis, if the presence of the latter is suspected, or to the 
toxic cause, if any is discoverable. 



INFERIOR POLIOENCEPHALITIS. 

(Progressive Bulbar Paralysis; Labio-glosso-laryngeal Paralysis.) 

Etiology. — Disease of the nuclei and lower neurons of the 
seventh, ninth, tenth, eleventh, twelfth, and the motor portion 
of the fifth cranial nerves may be due to: 

1. Extension of the degenerative process attending polio- 
myelitis (polioencephalomyelitis), locomotor ataxia, dissemi- 
nated sclerosis, syringomyelia, and descending degeneration 
of the pyramidal tracts following cerebral lesions. 

2. Toxemia, induced either by such diseases as syphilis,, 
diphtheria, or chronic nephritis; or by chemicals, such as lead- 
Symptoms. — The disease is insidious but progressive. As a 

rule, the tongue is first affected, and gradually becomes para- 
lyzed and atrophic, lying motionless in the mouth. Soon after 
this the lips are similarly involved, then the palate, the 
pharynx, and finally the larynx. Pronunciation becomes thick 
early in the course of the disease, and speech is gradually lost. 
The mouth drops open, and from it the saliva drules. Mas- 
tication becomes feeble or impossible, fluids regurgitating 
through the nose Involvement of the pharynx leads to diffi- 
culty in deglutition, food being apt to enter the respiratory 
tract, and the pharyngeal paralysis completely extinguishes the 
voice. Respiratory and cardiac failure may occasion the fatal 
termination at any time; but frequently it is precipitated by an 
aspiration-pneumonia or by asphyxia induced by obstruction 
of the respiratory passage by a mass of food.. 

Acute bulbar paralysis may develop in connection with 
acute myelitis; the symptoms are identical with those of the 
chronic form, but are rapidly evolved, and death from re- 
spiratory failure quickly follows. 



DISEASES OF THE NERVOUS SYSTEM. 411 

Prognosis. — The disease progresses steadily to a fatal termi- 
nation, usually within a few years. In the acute form death 
is almost immediate. 

Treatment. — In order to avoid asphyxia, the use of the 
stomach tube or rectal alimentation usually becomes neces- 
sary. Faradism may be applied to the paralyzed muscles, 
and such medicines as argentum nit., causticum, mercury y 
phosphorus, plumbum, and zinc may be tried. 

INFANTILE CEREBRAL PALSIES. 

Etiology. — Paralyses in childhood, the result of lesions of the 
upper neuron within the cranium, may be divided into : 

1. Paralyses of pre-natal onset. These may be due to actual 
deficiency of brain elements {agenesis), to imperfect develop- 
ment of the pyramidal tracts, or to gross cerebral defects 
{porencephalia). Injuries and diseases of the mother are 
doubtless important factors in the production of these lesions. 

2. Birth palsies. Injury to the fetal head by protracted or 
precipitate labor, or by the use of forceps, is the predominant- 
cause of this class of palsies, most of which are due to menin- 
geal, rarely cerebral, hemorrhage. 

3. Postnatal palsies. At this period the lesions are the same 
as in adults, i. e., hemorrhage, embolism, thrombosis, enceph- 
alitis, etc. Acute infectious diseases, convulsions, and trau- 
matism play an important etiologic part. 

Symptoms. — A majority of the pre-natal and natal palsies 
are diplegic in distribution, while those of post-natal origin are 
hemiplegic. In the diplegic cases the lower limbs are more 
seriously affected than the upper, and the face often escapes ; 
but mental impairment, often extreme, is usually associated. 
These children are inactive at birth, and rigidity and contract- 
ures may be detected during the early months of life. Athe- 
toid movements and epileptic convulsions develop in many 
of them. A certain variety of cases, due to premature birth 
and consequently defective development of the p3 T ramidal tract, 



412 DISEASES OF THE NERVOUS SYSTEM. 

are characterized by spasticity of the lower limbs without 
mental impairment {Little s disease). 

In the post-natal cases, the child is usually seized during an 
acute febrile attack with a convulsion more or less unilateral 
in its distribution. This is prolonged over several hours or 
else recurs several times, and during this period the child 
generally remains unconscious. Later the loss of power on 
one side is detected. Speech is temporarily lost, but is often 
regained with surprising rapidity. The paralyzed limbs soon 
become markedly spastic, the reflexes are exaggerated, and 
contractures and choreoid or athetoid movements develop. 
Imbecility and epilepsy are common sequels. 

Diagnosis. — The normal electrical reactions, normal trophic 
condition, and the subsequent spasticity serve to distinguish 
these cases from those due to cord lesions. 

Prognosis. — Complete recovery is impossible. The prob- 
ability of the avoidance of epilepsy and imbecility is better in 
the hemiplegic than in the diplegic cases, but in no case can 
even that be promised. 

Treatment. — The management of the apoplectic attack and 
the paralytic state is the same as that for similar conditions in 
adults. Surgical intervention may be practicable when the 
location of a meningeal hemorrhage is fairly localizable; and 
later, correction of deformities by apparatus or tenotomy is 
often advisable. In addition, nutrition must be maintained 
by careful dietetic measures and such constitutional remedies 
as aiirum, baryta carb., calcarea carb., cdusticum, lycopodium, 
mercury, and sulphur. For control of the mental enfeeble- 
ment education alone is effective. 

PARALYTIC DEMENTIA. 

(Paresis; General Paralysis of the Insane.) 

Etiology. — Intellectual overwork and strain acting upon a 
constitution often already weakened by alcoholism and espe- 
cially by syphilis (70%) are the usual causes of paresis. 



DISEASES OF THE NERVOUS SYSTEM. 413 

Pathology. — The process is a diffuse meningoencephalitis, in 
the course of which the brain becomes atrophied, especially its 
frontal lobe, and the meninges inflamed and thickened. The 
ganglion cells and nerve fibres are degenerated and in part 
destroyed. 

Symptoms. — The course of the disease is divisable into three 
periods, viz. : 

The Prodomal Period. The patient appears to be neuras- 
thenic, but in addition his conduct becomes "peculiar." He 
may be guilty of little lapses of memory, making slight errors 
in speaking or writing, or misusing words; or he ma} T offend 
the proprieties and show a tendency to alcoholic or sexual 
excesses. The patient early inclines to exaggerate his self- 
importance, and plunges into extravagant and impossible 
schemes, neglecting his legitimate business. Slight motor 
inco-ordinations, tremor of the facio-lingual muscles, and slur- 
ring articulation may be noted at this stage, which merges 
gradually into — 

The Period of Developed Dementia. Speech becomes stam- 
mering, the writing is marked by elisions and repetitions of 
words or syllables, tremor of the face and tongue is marked, the 
pupils are myotic, unequal, or insensitive, and do not respond to 
light, and the tendon reflexes are either lost or enormously 
exaggerated. The patient becomes weak and emaciated, and 
his mental state is marked by failure of memory and weak- 
ened judgment, loss of ethical and esthetic feeling, and emo- 
tional excitability; while the delusions which now develop are 
remarkable for their great exaggeration, whether of exaltation 
or depression. Most characteristic are the delusions of grand- 
eur; he imagines himself the greatest, the wealthiest, or the 
strongest man in the world. During this period the patient is 
seized with apoplectic or convulsive attacks, and the onset of 
the latter is followed by more rapid and apparent mental 
failure. 

The terminal stage supervenes. Memory fails, speech be- 
comes a jargon, the convulsions increase in frequency, and the 



414 DISEASES OF THE NERVOUS SYSTEM. 

patient becomes helpless and bed-ridden, and finally exhaus- 
tion or intercurrent disease induces the fatal termination. 

Diagnosis. — In the early stage it is important to exclude 
neurasthenia and hypochondriasis, and this is usually possible 
by noting the alteration in character, the speech defect, the 
tendency to motor inco-ordination, and the pupillary changes. 
Cerebrospinal syphilis is more sudden in onset, headache, 
often nocturnal, is more frequent and severe, affections of 
tongue and speech are wanting,, paralytic symptoms appear 
earlier, the mental symptoms are not characteristic, and de- 
lusions of grandeur are lacking. 

Prognosis. — The prognosis is hopeless, death usually occurring 
within five years from the onset and often within three. 

Treatment. — The patient should be placed in charge of a 
trained attendant who will supervise his diet, cleanliness, and 
general hygiene, and if possible he should be sent away from 
home. If any suspicion of syphilis exists, an anti-syphilitic 
treatment should be carried out. Of medicines, argentum nit., 
arsenic, aurum, belladonna, hyoscyamus, platina, secale, and 
stramonium may be symptomatically useful. 

DISSEMINATED CEREBROSPINAL SCLEROSIS. 

(Insular Sclerosis; Multiple Sclerosis.) 

Etiology. — This disease is usually secondary, the principal 
factors in its production being: 

1. Infection. In a large proportion of cases the disease de- 
velops soon after one of the acute infectious fevers. 

2. Intoxication. Lead, copper, and zinc are said to induce 
the sclerotic changes. The disease usually appears between 
the ages of twenty and thirty years. Heredity, traumatism, 
excesses, etc., may have some predisposing influence. 

Pathology. — The irritative cause, whatever its nature, reaches 
the central nervous system through the blood and there sets 
up localized degenerative processes. As a result, scattered 
patches of sclerosis develop irregularly through the white and 
gray matter of the brain, cord, and spinal nerves. 



DISEASES OF THE NERVOUS SYSTEM. 415 

Symptoms. — In spite of the irregular and scattered lesions, 
the symptoms are fairly uniform, viz., 

1. Intention tremor, i. e., a coarse tremor which disappears 
while the extremity is at rest, but reappears and augments 
while movement is going on, is almost pathognomonic of the 
disease. 

2. Nystagmus is present in two-thirds of the cases. 

3. Scanning speech, a peculiar defect in articulation due to 
separation and accentuation of the syllables of each word, is a 
common, symptom. 

4. Mental enfeeblement in various degrees can usually be 
detected. 

5. Amblyopia, due to optic neuritis or atrophy, is ver} 7 com- 
mon. Paretic conditions of the eye muscles and pupillary 
changes are also frequently present. 

6. Motor weakness is usually detectable. The gait may be 
spastic, or it maybe of cerebellar type, i. e., staggering. The 
reflexes are generally exaggerated, and clonus may be discov- 
ered. 

Apoplectiform attacks, transitory hemiplegias, and vertigo 
may mark the course of the disease. General sensibility is not 
affected, and visceral and trophic disturbances are almost un- 
known. 

Diagnosis. — The intention tremor, scanning speech, nystag- 
mus, and irregularities of gait usually render diagnosis easy. 
Hysteria may be distinguished by its stigmata. 

Prognosis. — The course of the disease is apt to be prolonged 
over a period of years. Occasionally it reaches its full develop- 
ment in a few months, and in some cases only a few of the 
symptoms ever appear ( formes frustes). It may terminate in 
dementia, or death may be due to intercurrent disease, apo- 
plectiform attacks, or bulbar involvement. 

Treatment. — Attention should be paid to the control of infect- 
ive processes, general nutrition should be preserved, and inter- 
nally such remedies as aurum, mercurius, plumbum, and zinc 
may be used. 



416 DISEASES OF THE NERVOUS SYSTEM. 

DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 
SPINAL PACHYMENINGITIS. 

Etiology. — The inflammation may take place in the loose 
cellular tissue separating the dura from the bony wall {external 
pachymeningitis) . This is always secondary to disease of the 
vertebrae (Pott's disease), or to inflammatory processes nearby 
(abscesses, bed sores, etc.). Inflammation of the inner layer 
of the dura {internal pachymeningitis) may be hemorrhagic 
(hematoma) or hypertrophic, the latter representing simply 
the thickening and hypertrophy resulting from organization of 
the effused blood. The process may be extensive or it may be 
confined to a comparatively small arterial area, especially in 
the cervical region {pachymeningitis cervicalis hypertrophica), 

Symptoms. — External Pachymeningitis gives rise to local 
tenderness over the spine, pain, muscular twitchings, and 
cutaneous hyperesthesia in the area of distribution of the 
affected nerves. 

Internal Pachymeningitis is slow in onset, beginning 
with pain over the affected area of the spine and in the 
peripheral distribution of the corresponding nerves. In the 
course of months this is followed by loss of power, atrophy, 
and anesthesia in these areas, together with spastic symp- 
toms, rigidity, and increased reflexes in the lower extremities, 
due to degeneration of the lateral tracts following compression 
of the cord. 

Diagnosis. — External pachymeningitis is distinguished from 
myelitis by the preponderance of pain, spasm, and irritation 
over paralysis, and by discovery of the causative disease. 

Internal pachymeningitis can be distinguished from amyo- 
trophic lateral sclerosis by the presence of severe pain in the 
back and arms, and from syringomyelia by the absence of the 
peculiar sensory changes of that disease. It may be difficult 
to exclude tumor. 

Treatment. — The treatment of either form of pachymenin- 



DISEASES OF THE NERVOUS SYSTEM. 417 

gitis, except in cases of syphilitic origin, is surgical. That asso- 
ciated with Pott's disease is least grave, owing to the success 
of orthopedic measures in controlling the latter disease. In 
the other cases surgical intervention, though hazardous, offers 
almost the only hope. In acute cases the use of aconite, bella- 
donna, Bryonia, or hepar is often indicated. In cases depend- 
ent upon vertebral caries, calcarea, fluoric acid, silica, and 
sulphur may be prescribed. Syphilitic cases require mercury 
or an iodide. 



SPINAL LEPTOMENINGITIS. 

Etiology. — Acute inflammation of the pia mater is due to in- 
fection occurring in connection with acute infectious fevers, 
tuberculosis, syphilis, etc., or to extension of a contiguous in- 
flammation. 

Pathology. — The membrane becomes hyperemic and the 
pia-arachnoid space is filled with a sero-fibrinous or purulent 
exudate. If recovery follows, the inflammatory exudate is 
gradually absorbed and a diffuse thickening of the meninges 
persists, with adhesions between the membranes (chronic 
meningitis). 

Symptoms. — The disease begins abruptly, a sharp chill being 
followed by intense pain in the back, which radiates around the 
body and down the limbs. There is tenderness over the spine, 
and rigidity and spasm of the muscles, causing stiffness of the 
neck and back and even opisthotonos. Vomiting and convul- 
sions may occur. Medullary involvement may cause dyspnea, 
Cheyne-Stokes respiration, and cardiac failure. At first the 
reflexes are increased. Should the patient outlive the acute 
symptoms, paralysis, anesthesia, atrophy, and contractures 
will develop in those regions of which the nerve supply is 
affected. 

The chronic form presents the symptoms of the acute in 
lessened intensity, pain in the back predominating. Complete 
recovery is rare. 

07 



418 DISEASES OF THE NERVOUS SYSTEM. 

Diagnosis. — The sudden onset of pain in the back, rigidity, 
hyperesthesia, and irregular temperature and pulse serves to 
distinguish the disease. Myelitis is characterized by paralysis 
and lack of pain, but a certain degree of myelitis frequently 
accompanies acute leptomeningitis. Subdural hemorrhage 
presents similar symptoms, but is extremely abrupt in onset, 
usually following strain or traumatism. Hemorrhage into the 
spinal cord is followed instantly by paralysis, sometimes with- 
out pain. Tetanus is distinguished by early trismus, fever, 
paroxysms of spasm, intense hyperesthesia, and a history of 
traumatism. 

Prognosis. — The outlook is grave, some cases terminating in 
death within two days, others in a week or two; while in those 
that survive some degree of paralysis usually persists. An 
acute onset, virulent infection, high temperature, and implica- 
tion of the upper cord are unfavorable signs. 

Treatment. — Place the patient at absolute rest on his side 
and apply heat or ice bags to the spine. Warm baths are of 
service in some cases. Aconite may be given at the onset, 
but the developing inflammation soon requires belladonna^ 
bryonia, or rhus tox. Apis, causticum, cuprum, hypericum^ 
oxalic acid, secale, and veratrum viride, have also been used 
with success. 

SPINAL HEMORRHAGE. 

Etiology. — The hemorrhagic effusion may be extra-meningeal 
(between the dura and the spinal canal), intra-meningeal (be- 
tween the dura and the arachnoid), or into the substance of the 
cord. In the majority of cases it is due to traumatism. In 
others, rupture of an aneurism, erosion of an artery (caries, 
carcinoma), or altered blood states (hemophilia, purpura, or 
those accompanying infectious disease) are responsible for the 
hemorrhage. Intra-medullary hemorrhage may be secondary 
to myelitis, meningitis, syringomyelia, etc. 

Symptoms. — The symptoms are more or less sudden in onset, 
and consist of pain in the back, accompanied by numbness or 



DISEASES OF THE NERVOUS SYSTEM. 419 

tingling. If the hemorrhage is meningeal in location, irrita- 
tive symptoms (hyperesthesia, paresthesia, neuralgic pains, 
etc.) may be present ; and later, or at the time of onset if the 
lesion is within the cord, paralysis, usually paraplegia, de- 
velops. Consciousness is preserved during the attack. Symp- 
toms of myelitis may ensue. 

Diagnosis. — The diagnosis rests upon the sudden onset of the 
irritative or paralytic phenomena, without loss of conscious- 
ness. 

Prognosis. — This is unfavorable. Death is not unusual, especi- 
ally if the cord-substance is involved; and at best some degree 
of permanent paralysis will remain. Exceptionally a clot, if 
very small, may be absorbed and recovery ensue. 

Treatment. — Place the patient at rest, apply an ice bag to the 
spine, and administer aconite, arnica, hamamelis, or veratrum 
vir. In general, treat the case as one of intracranial hemor- 
rhage. 

ACUTE ASCENDING PARALYSIS. 

(Landry's Paralysis. ) 

Etiology. — This is a rare disease of unknown causation. It 
appears to follow closely upon various infectious diseases 
(small-pox, typhoid, influenza, diphtheria, syphilis, etc.), and 
is probably of toxemic origin. 

Pathology. — Myelitic softening of varying extent ■ occurs in 
the gray matter and the adjacent white fibres of the dorsal 
and cervical cord, and is accompanied by degeneration in the 
root fibres and peripheral nerves. The spleen is enlarged and 
softened, and the lymphatic glands are engorged. 

Symptoms. — A sensation of weakness begins in the feet and 
slowly creeps upward through the legs into the trunk and 
finally the upper limbs. The parts quickly become paralyzed 
in the order of involvement, and in the course of two or three 
days difficult respiration, due to paralysis of the diaphragm, 
and difficulty in deglutition may appear. In severe cases 
every voluntary muscle below the face may be paralyzed. In 



420 DISEASES OF THE NERVOUS SYSTEM. 

a few cases the upper limbs are first involved, the paralysis 
spreading downward. The paralysis may stop at any point 
and then recede. Sensation is normal. The reflexes are 
abolished. 

Diagnosis. — The diagnosis rests upon: 

1. The mode of invasion. 

2. The purely motor paralysis. 

3. The absence of sensory symptoms and of changes in 
electrical irritability. 

In ordinary myelitis the cord functions below a certain level 
are involved, and sensory symptoms, sphincteric paralysis, 
and the reaction of degeneration are present. In acute anterior 
poliomyelitis the paralysis reaches its height at once and then 
tends to recede, and the reaction of degeneration is present. 

Prognosis. — The prognosis is unfavorable, the vast majority 
of cases terminating through bulbar involvement within a few 
days. Exceptionally, spontaneous arrest is followed by re- 
covery. 

Treatment. — Place the patient at absolute rest, nourish him 
with easily assimilable food, and administer aluminum, coc- 
culus, conium, gelsemium, ledum, rlius tox., or secale. 

MYELITIS. 

Etiology.- -Acute inflammation of the cord substance may be 
due to: 

1. Injuries to the spinal column (fracture, caries, etc.). 

2. Injuries to the cord itself (wounds, lacerations, hemor- 
rhages, compression by tumors, etc.). 

3. Infectious diseases (syphilis, rarely small-pox, typhoid, 
septicemia, etc.). 

-I. Involvement of the cord by extension of a meningeal 
inflammation. 

5. Exposure to cold and wet, and excessive physical exer- 
tion act, if at all, by lessening resistance. 



DISEASES OF THE NERVOUS SYSTEM. 421 

Pathology. — The cord becomes reddened and soft, the out- 
line of the gray matter appearing indistinct. The whole 
thickness of the cord may be involved {transverse myelitis'), 
a large vertical section may be inflamed {diffuse myelitis), or 
the lesion ma}' limited to the central gray matter {central my- 
elitis). Secondary degenerations ensue in — 

(1) The lateral column below the lesion, and 

(2) The posterior column and direct cerebellar tract above 
the lesion. 

Symptoms. — The symptoms vary according to the causative 
lesion and the part of the cord involved. The symptoms com- 
mon to all localizations are: 

1. Motor paralysis. Paraplegic weakness develops either 
suddenly or gradually, and as a result the patient is incapable 
of actively moving his legs. 

2. Motor irritation. Muscular twitchings occur in the 
paretic limbs. 

3. Sensory disturbances. A band of hyperesthesia surrounds 
the trunk at the upper level of the cord lesion; it is due to irri- 
tation, and is often associated with a "girdle sensation." 
Below this zone sensation is more or less blunted, and anesthe- 
sia, paresthesia, or hyperesthesia may be present. 

4. Changes in the reflexes. Those reflexes whose spinal 
centres are involved by the lesion are abolished. Below that 
level, unless the cord is actually divided, they are at first dimin- 
ished, but later they become greatly exaggerated and are asso- 
ciated with rigidity and clonus. 

5. Disturbances of Bladder and Rectum. There ma}* be, 
early, retention and constipation, but as a rule incontinence of 
both urine and feces ensues. 

6. Trophic changes. The muscles innervated from the de- 
stroyed cord-segment undergo atrophy and exhibit the re- 
action of degeneration. The inert limbs ma}' lose in size 
from disuse, but the electrical reactions are unchanged and 
the reflexes are increased. The general vasomotor and trophic 
conditions are disturbed, however, and as a result the paralytic 



422 DISEASES OF THE NERVOUS SYSTEM. 

extremities are cold and cyanotic, the skin is harsh, and bed- 
sores are frequent. 

Diagnosis. — The location of the lesion may be determined by 
the distribution of the paresis and the level of the hyperes- 
thetic zone. Acute poliomyelitis is without sensory disturb- 
ance; in meningitis, spinal tenderness is marked, the girdle 
pain is absent, and the sphincters are unaffected; in multiple 
neuritis the onset is slow, there is pain along the affected 
nerves, and the bladder and rectum are not involved; and in 
hysteria the sensory disturbance is characteristic in outline, 
and no muscular atrophy, bedsores, or sphincteric paralysis is 
present. 

Course and Prognosis. — Acute cases reach their height in a few 
days, and if death does not occur at once, there is a prolonged 
stationary period, or a gradual improvement or decline. 
Chronic myelitis differs only in the period required for its de- 
velopment. In any case the prognosis is grave, those that 
survive the inflammatory period often becoming hopelessly 
paraplegic, and ultimately perishing from exhaustion or inter- 
current disease. In a few cases, however, almost complete 
recovery takes place. Cervical myelitis is almost invariably 
fatal, and involvement of the lumbar enlargement is disastrous 
because of its permanent effects on the sphincters and legs. 
Acute cystitis and bedsores are unfavorable omens. 

Treatment. — Place the patient at rest, and endeavor to pre- 
vent bedsores by absolute cleanliness, alcohol baths followed 
by thorough drying, and frequent changes of position. Cathe- 
terization, should it become necessary, must be guarded by 
strict asepsis. The supervention of cystitis requires that the 
bladder be washed out. Electricity may be used after acute 
symptoms have subsided. The principal remedies are arnica 
and Hypericum in traumatic cases, and rJius tox. or dulcamara 
in those following exposure. Arsenic, belladonna, cuprum 
arsen., ergot, mercury, and strychnia are also recommended. 



DISEASES OF THE NERVOUS SYSTEM. 423 

ACUTE ANTERIOR POLIOMYELITIS. 

(Atrophic Spinal Paralysis; Infantile Spinal Paralysis, etc.) 

Etiology. — This acute myelitis of the anterior horns is prob- 
ably of an infective nature; it occurs mostly in children under 
ten years of age, and occasionally becomes epidemic. 

Pathology. — The sudden paralysis is the result of intense con- 
gestion of the anterior cornua. Subsequently softening, usually 
unilateral, leads to destruction of the multipolar ganglion 
cells, and so causes a certain degree of permanent paraly- 
sis and atrophy. Frequently several foci of myelitis are pres- 
ent at different levels. Ultimately these areas are replaced by 
connective tissue, and the anterior nerve roots and the muscles 
themselves become degenerated. 

Symptoms. — Without prodromes a child becomes ill and fever- 
ish (100°-102°), and in the course of a few hours a flaccid 
paralysis of one or more of the extremities is noticed. This 
remains stationary for a few days or several weeks and then 
gradually declines, but leaves certain muscle-groups perma- 
nently paralyzed. The lattersoon become atrophied and show 
the reaction of degeneration. Ultimately the growth of the 
associated bones may be retarded, and the muscular paralysis 
permits various distortions to develop. Sensation is un- 
affected, and the bladder and rectum are not involved. 

Diagnosis. — The sudden appearance of the paralysis should 
render diagnosis easy. Infantile cerebral paralysis is almost 
always ushered in by convulsions limited to one side of the 
body; convulsions may occur in poliomyelitis as in other 
febrile diseases of childhood, but they are generalized. The 
absence of sensory disturbances, bedsores, and sphincteric 
involvement will exclude myelitis. In severe neuritis sensory 
disturbances are present, and the disease is less acute in its 
onset. 

Prognosis. — A fatal termination is rare, and to a certain degree 
the paralysis will recede, but a portion of the latter is apt to 



424 DISEASES OF THE NERVOUS SYSTEM. 

be permanent. Those muscles which at the end of two weeks 
show even a slight response to faradism will certainly recover; 
the others probably will not. Progressive muscular atrophy 
may develop later in life. 

Treatment. — Place the patient at rest, wrap the paralyzed 
limbs in cotton, and prescribe belladonna or gelsemium. When 
the paralysis begins to subside, place a positive electrode over 
the spine and with the negative electrode apply a mild gal- 
vanic current for several minutes daily. Sustain the child's 
general nutrition with proper food and fresh air, and prescribe 
medicines according to the constitutional indications present. 



CHRONIC ANTERIOR POLIOMYELITIS' 

(Spinal Form of Progressive Muscular Atrophy) 

Etiology. — The cause is practically unknown, although the 
disease has been attributed to excessive muscular activity, ex- 
posure to cold, infectious diseases, and lead poisoning. 

Pathology. — The large multipolar cells in the anterior horns 
of the gray matter in the cord become degenerated and de- 
stroyed, and as a result the entire lower motor neuron degen- 
erates and the muscular tissue which it supplies becomes flaccid 
and undergoes atrophy. Sclerotic changes also occur in the 
lateral tracts ; if sufficiently marked to cause symptoms, the 
disease becomes amyotrophic lateral sclerosis (q. v.) 

Symptoms. — The principal manifestation of the disease is a 
slowly progressive muscular atrophy. Usually it begins in the 
upper extremities (Aran-Duchenne type), affecting first the 
muscles of the one hand, the thenar (thumb) and hypothenar 
(little finger) eminences wasting, and the interossei under- 
going atrophy, so that the hand becomes claw-like {main en 
griff e). The other hand becomes involved later. Sometimes 
the wasting begins about the shoulder first, but in any case it 
soon involves the other muscles of the back, especially the 
trapezii and sometimes the respiratory muscles. Less often 
the atrophy commences in the legs, the gluteal muscles, the 



DISEASES OF THE NERVOUS SYSTEM. 425 

vasti, and the anterior tibials being first attacked. In other 
cases the atrophy begins in the peronei, later involving the 
calf and thigh muscles {peroneal, leg, or Charcot-Marie type). 
The face usually escapes. 

As the result of the atrophy, muscular power fails, fibrillary 
twitchings may be observed, and galvanic and faradic irrita- 
bility becomes progressively diminished. The reflexes are lost, 
but the special senses and the sphincters are not affeeted. 

Diagnosis. — The diagnosis rests upon the appearance of wast- 
ing in one group of muscles after another, with accompanying 
loss of power, fibrillary twitchings, changed electrical reactions, 
and loss of reflexes. Amytrophic lateral sclerosis is distin- 
guished by a more rapid course, together with increased re- 
flexes and spasticity. Muscular dystrophics begin in childhood, 
are slower in progress, more frequently involve the lower limbs, 
the electrical responses are unaltered, and fibrillary twitching is 
absent. Neuritis is more rapid in onset, is usually accom- 
panied by pain, and has no progressive tendency. Syringo- 
myelia presents peculiar trophic and sensory phenomena. 

Prognosis. — The course of the disease is prolonged, and it is 
rarely checked. In the course of years bulbar involvement or 
invasion of the respiratory muscles may precipitate a fatal ter- 
mination. 

Treatment. — Moderate exercise in the open air and good 
food are necessary. Galvanism may be applied to the spine 
daily, and such remedies as arnica, arsenic, cuprum, gelsemium, 
mercurius, phosphorus, physostigma, and sulphur may be pre- 
scribed. 

Strychine nit., in hypodermatic doses of gr. T ^-o, increased 
to gr. 4V, daily, is said to arrest the progress of the disease. 

AMYOTROPHIC LATERAL SCLEROSIS. 

Etiology. — The cause is unknown. 

Pathology. — Degeneration of the pyramidal tracts in the cord 
(upper motor neuron) is associated with destruction of the 
ganglion cells in the anterior horns and medulla (lower 



426 DISEASES OF THE NERVOUS SYSTEM. 

motor neuron) with consequent atrophy of the muscles de- 
pendent upon the latter. Other portions of the cord are some- 
times slightly involved. 

Symptoms. — The disease is characterized by a combination of 
the symptoms of progressive muscular atrophy and spastic 
paraplegia, viz., 

1. Progressive muscular wasting and a corresponding de- 
gree of motor weakness. As a rule these atrophic symptoms 
appear first in the upper extremities, involving the muscles in 
the order described as usual in cases of chronic anterior 
poliomyelitis. Fibrillation and diminished electrical irrita- 
bility can be detected. 

2. Rigidity, increased reflexes, and sometimes contractures. 
These spastic symptoms usually appear in the lower ex- 
tremities, giving rise to a characteristic spastic gait. The 
sphincters are unaffected and cutaneous sensibility is normal. 

Diagnosis. — The exaggerated reflexes and spastic phenomena 
serve to distinguish the disease from chronic anterior polio- 
myelitis. 

Prognosis.— Hopeless. Death will probably result from ex- 
haustion or bulbar involvement within two or three years. 

Treatment. — Rest, massage, and such remedies as argentum 
nit., arsenic, lathy rus, plumbum, and strychnine. 



SPASTIC PARAPLEGIA. 

(Lateral Sclerosis; Spastic Spinal Paralysis.) 

Etiology. — Degeneration of the pyramidal tracts may follow 
a lesion of the upper neuron situated at any point between the 
motor cortex and the spinal termination of the axon. Occurring 
bilaterally the condition may be secondary, therefore, to any 
transverse lesion of the cord above the lumbar enlargement. 
In rare cases it may be primary. 

Symptoms. — The condition is of very gradual onset, the prin- 
cipal symptoms being — 



DISEASES OF THE NERVOUS SYSTEM. 427 

1. Weakness of the lower extremities, which gradually 
progresses to total disability. The arms are rarely involved. 

2. Rigidity in the muscles of the lower extremities. This 
spasticity corresponds to the degree of paralysis. The tendon 
reflexes are greatly exaggerated and ankle clonus can be ob- 
tained. 

The "spastic gait" is characteristic; the patient moves his 
legs as a whole without bending them, and the toes scrape the 
ground. In children there may be "cross-legged progression," 
because of spasm of the abductors. There is little or no 
sensory disturbance or muscular atrophy, the electrical reac- 
tions are normal, and the sphincters are seldom affected. 

A hereditary spastic paraplegia has been described, notably 
by Bayley, who traced a series of cases through five genera- 
tions. Spasticity and increased reflexes were the essential 
phenomena. 

Diagnosis. — The association of spasm with motor paralysis 
furnishes a diagnosis of the condition, but only when a careful, 
persistent search for a causal lesion has been in vain can the 
disease be considered primary. 

Hysterical paraplegia usually presents some rigidity, but it 
is not true spasticity and the knee jerk is not so markedly ex- 
aggerated, nor can clonus be obtained. Ataxic paraplegia is 
distinguished by inco-ordination; amyotrophic lateral sclerosis, 
by muscular atrophy. 

Prognosis. — Recovery is impossible and improvement is ex- 
ceptional. 

Treatment. — Rest, massage, and the administration of such 
medicines as argentum, lathyrus, nux vomica, phosphoriis,' 
strychnine, and zinc. 

ATAXIC PARAPLEGIA. 

(Combined Sclerosis; Postero-lateral Sclerosis; Progressive Spastic Ataxia.) 

Etiology. — Simultaneous degeneration of the lateral and pos- 
terior columns is usually secondary, especially to— 



428 DISEASES OF THE NERVOUS SYSTEM. 

1. Locomotor ataxia, an associated myelitis involving the 
lateral tracts. 

2. Paralytic dementia, by a similar extension. 

3. Diffuse myelitis, giving rise to ascending degeneration of 
the posterior and descending degeneration of the lateral tracts. 

4. Leptomeningitis, an associated myelitis involving the 
periphery of the cord. 

5. Vascular lesions, sclerosis of the lateral and posterior 
tracts being secondary. 

6. Embryonic deficiency. 

Exposure, traumatism and syphilis are sometimes credited 
with inducing the disease. 

Pathology. — The process begins in the lumbar region, and the 
posterior and lateral columns are both affected, but with un- 
equal intensity. The posterior root zone usually escapes. 

Symptoms. — The symptoms are, roughly speaking, those of 
spastic paraplegia and ataxia combined. The esssential char- 
acteristics of the disease are: 

1. Ataxia, especially of the lower extremities. 

2. Gradual loss of power in the lower extremities with spastic- 
ity and increased reflexes. Some cases show a preponderance 
of spasticity, while others incline more to the tabetic type, 
with loss of sexual power, sphincteric paresis, girdle sensation, 
dull aching, and more rarely lightning pains, Argyll-Robert- 
son pupil, and even loss of the knee jerk. 

Diagnosis. — The diagnosis rests upon the association of ataxia 
with muscular weakness and spasticity. 

Prognosis. — The disease is slowly progressive, death occurring 
eventually, as in other spinal degenerations, as the result of 
cystitis, bed sores, or intercurrent disease. 

Treatment. — That of locomotor ataxia. 



DISEASES OF THE NERVOUS SYSTEM. 429 

FRIEDREICH'S ATAXIA. 

(Hereditary Ataxia.) 

Etiology. — This degenerative disease of the posterior and 
lateral columns, which is thereby closely related to ataxic 
paraplegia and locomotor ataxia, usually attacks several chil- 
dren of one family, appearing before adolescence. In some 
cases, generally those appearing after puberty, the cerebellum 
is involved (hereditary cerebellar ataxia). 

Symptoms. — The principal symptoms are: 

1. Ataxia. The child is very unsteady on its feet, stum- 
bling, staggering, and reeling. The movements of the arms 
become unsteady and jerky, and tremor and choreiform move- 
ments may be noted. Ultimately even the head becomes 
involved. 

2. Speech disturbance. Inco-ordination renders speech jerky 
or hesitating, with elision of certain syllables; and the pitch 
changes suddenly at times. 

3. Nystagmus. Frequently this oscillation develops only 
when the eyes are directed laterally or upward. 

4. Changes in the deep reflexes. In cases of the spinal type 
the knee jerk is lost early; in the rarer cases of cerebellar 
type, the deep reflexes are exaggerated and clonus may be 
associated. 

5. Muscular strength is but slightly reduced. Late in the 
disease club-foot and lateral spinal curvature may develop. 

Diagnosis. — The hereditary character of the disease and its 
onset in early life are usually distinctive. Ataxic paraplegia 
lacks the nystagmus and defective articulation. Disseminated 
sclerosis may be distinguished by its intention tremor, its lack 
of static ataxia, its scanning speech, and its spastic features. 

Prognosis.— The disease is incurable but runs a protracted 
course, extending over many years. 

Treatment. — This is very unsatisfactory. Galvanism, spinal 
stretching, and prescribed exercises may be tried. 



430 DISEASES OF THE NERVOUS SYSTEM. 

LOCOMOTOR ATAXIA. 

(Tabes Dorsalis; Sclerosis of the Posterior Columns.) 

Etiology, — The principal and perhaps the only factor in the 
production of locomotor ataxia is syphilis (90%), the disease 
usually appearing from five to fifteen years after the initial 
lesion. As a natural corollary, it is a disease principally of 
adult males. 

Pathology.— The syphilitic toxin primarily affects the cell- 
bodies of the afferent sensory fibres, with ensuing degenera- 
tion in the peripheral nerves, the posterior roots, and the 
posterior columns of the cord, and with the latter meningitis 
may be associated. Similar changes may occur in the medulla 
and the brain, the latter constituting paralytic dementia. 
These degenerative changes are sclerotic in nature and irrep- 
arable (parasyphilitic). 

Symptoms. — The more important symptoms of tabes are as 
follows: 

1. Disturbances due to loss of the muscular sense. As a re- 
sult of this the patient cannot determine the position of his 
limbs, and is unable to co-ordinate his movements. I^arly he 
presents static ataxia (Romberg's sign), swaying or falling when 
he attempts to stand with closed eyes. Later the ataxic gait 
develops; the patient's movements are unsteady, the foot is 
raised too high, thrust forward too far, and comes down flat 
with a slap. In time it becomes necessary for him to use one 
or two canes and to watch his feet while he walks, and 
ultimately walking, even with these aids, is impossible. The 
upper extremities may become markedly ataxic, the patient 
being unable to touch his nose, ear, or other object when his 
eyes are closed, and the ordinary movements of the arms 
becoming very inexact. Involuntary movements, consisting of 
sudden jerks of the extremities, are sometimes observed. 
Palsies, due to involvement of the anterior horn or to vas- 
cular changes in the cerebellum or cord, appear in a minority 
of the cases. They are usually mild and transitory. 



DISEASES OF THE NERVOUS SYSTEM. 431 

2. Sensory symptoms. The most important sensory disturb- 
ances are the lightning {fulgurant) pains, darting or stabbing" 
in character and lasting but a second or two. Frequently 
they are accompanied by more or less constant burning or 
tingling sensations. Pain is also associated with the various 
tabetic crises. Many patients complain of a sensation as of a 
tight belt about the trunk {girdle sensation), and in a majority 
of patients a band of anesthesia can be detected about the 
chest {tabetic cuirass). Either analgesia or hyperalgesia is apt 
to be present, and is usually of rather symmetrical distribution. 
Sensation is sometimes delayed, and even the syringomyelic 
dissociation of cutaneous sensibility may be encountered. 

3. Reflexes. The knee jerks are diminished, unequal or lost 
{WestphaV s sign) early, and the ankle jerk fails at the same 
time. Later the iris reflex to light is abolished, accommoda- 
tion remaining unaffected {Argyll-Robertson pupil). The or- 
ganic reflexes may be involved, with resulting loss of control of 
the sphincters ; and there is loss of sexual appetite, with more 
or less impotence. 

4. Visual Disturbances. In addition to the loss of the light 
reflex, many other ocular changes may occur in locomotor 
ataxia, notably atrophy of the optic nerve. Pupillary disturb- 
ances, ptosis, or squint may develop. 

5. Visceral Symptoms. Paroxysmal attacks of disturbed 
function and pain {tabetic crises) are very common. They 
may affect the stomach, causing vomiting and prostration; the 
intestine, causing diarrhea or constipation and often tenesmus; 
the urinary apparatus, causing intense colicky pains with great 
desire but inability to urinate; or the larynx, causing dyspnea 
and cough, and even cyanosis. 

6. Trophic disorders. The nutritional disturbance may lead 
to striking dystrophies, notably spontaneous fractures and ta- 
betic arthropathies {Charcot' s joints.) The latter are charac- 
terized by the rapid onset of a painless swelling, without red- 
ness or pufnness, about a joint. This may quickly subside, 
but in severe cases it becomes permanently localized in a 



432 DISEASES OF THE NERVOUS SYSTEM. 

globular form about the joint. There is a tendency to the 
recurrence of these attacks, with ultimate disintegration' of 
the articular structures, as a result of which the old tabetic 
joint may be a mere bag of bone fragments. A perforating 
painless ulcer, usually in the foot, is not uncommon; and many 
other less typical trophic changes may be present. 

Course. — The onset of tabes is insidious and its course slowly 
progressive, but three stages are described, viz., 

1. The Pre-ataxic Stage. — The chief symptoms at this 
period are lightning pains and loss of the knee jerk. The 
gait may be unaltered, but often there is static ataxia and an 
Argyll-Robertson pupil. 

2. The Ataxic Stage. — This cannot be sharply distinguished 
from the first stage, but is marked by the development of an 
ataxic gait. The early symptoms persist and become in- 
tensified, visceral crises and arthropathies appear, and sphinc- 
teric control is lost. 

3. The Paralytic or Terminal Stage. — The patient becomes 
unable to "use his legs" because of increasing ataxia, and is 
practically helpless. The previous symptoms continue and 
may be more fully developed. Cystitis, bulbar involvement, 
or some intercurrent disease may induce a fatal termination at 
any time. 

Diagnosis. — The diagnosis of a fully developed case, with 
lightning pains, loss of knee jerks, ataxia, and Argyll-Robert- 
son pupil, presents no difficulties. In the early stage the con- 
dition may be more obscure, but loss of knee jerk together 
with either static ataxia or lightning pains justifies a conclu- 
sion provided neuritis (q. v.) and anterior poliomyelitis can 
be excluded. In certain cases the disease begins in the cervi- 
cal region, and in consequence it is marked by little inco-ordi- 
nation or static ataxia and for a time the knee jerks may be 
retained. In such a case syringomyelia may be suspected, 
but as a rule the latter presents dissociation of cutaneous sensi- 
bility, local atrophies early in the disease, persistently in- 
creased knee jerks, and absence of inco-ordination. Para- 



DISEASES OF THE NERVOUS SYSTEM. 433 

plegias are usually accompanied by exaggerated reflexes and 
often clonus. 

Prognosis. — -Recovery is impossible, but in some cases the 
progress of the disease may be checked. Optic atrophy is 
often followed by arrest of the ataxic conditions. 

Treatment. — 1. Control any active syphilitic process. As a 
rule the luetic manifestations are past, but if they are still 
present, mercury and the iodides should be given. 

2. Preserve the general health. This implies attention to 
hygiene and diet. 

3. Increase the nutrition of the cord by daily suspension, 
using the Sayre apparatus, or, better, seat the patient on a 
table or on the floor and forcibly depress the head toward the 
knees and preserve this cord-stretching attitude for two min- 
utes. 

4. Systematic exercises aid in the preservation of muscular 
control. The patient should be encouraged to perform certain 
prescribed definite movements for a few minutes each day. 

5. Medicines. Argentum nit. is the remedy most often in- 
dicated in locomotor ataxia. Alumina, aurum, pJiosphorus y 
picric acid, seca/e, zinc, and zinc phosphide are useful at times, 
and a host of other drugs may be suggested by intercurrent 
symptoms. The severity of the lightning pains may some- 
times justify the use of analgesics (antipyriue or acetanilid, 
gr. v-x, rarely morphia, gr. -§— ^), but great caution must be ob- 
served in the repetition of such medicines. 

SYRINGOMYELIA. 

Etiology. — Syringomyelia appears to affect especially men 
who have been accustomed to hard labor. Exposure, trauma- 
tism, and the infectious diseases have been suggested as 
causes, but their relationship is purely conjectural. 

Pathology. — A gliomatous infiltration takes place around the 
central canal or in the gray horns of the cord, and subse- 
quently undergoes degeneration, forming cystic cavities. 
28 



434 DISEASES OF THE NERVOUS SYSTEM. 

Rarely a central myelitis or hemorrhage may lead to a similar 
excavation. The cavity lies in the gray matter and may be 
in the position of the central canal. Secondary degeneration 
may appear in the anterior or posterior columns or horns. 

Symptoms. — The symptoms may, according to the extent of 
the lesion, embrace changes in all the cord functions. The 
disease is of slow onset, beginning in early adult life, and is 
usually marked by the following symptoms: 

1. The temperature and pain senses are lost, while the tactile 
and muscular senses are preserved (the syringomyelic dissocia- 
tion). 

2. Muscular atrophy, varying in its location according to 
the portion of the cord diseased, is usually present. It is 
most frequent in the upper extremities, and is accompanied 
by fibrillary twitchings and the reaction of degeneration. 

3. Spasticity of the muscles develops when the lateral tract 
becomes involved. 

4. Trophic phenomena, such as glossy skin, hypertrophic 
nails, paronychia, herpetic and bullous eruptions, etc., are 
frequently seen. Arthropathies are almost invariably present, 
affecting the spine (scoliosis, angular deformities) and the 
articulations of the upper extremities by preference. 

The special senses and the sphincters are normal. 

Morvaii s disease is a clinical variety of syringomyelia in 
which the latter is probably complicated by peripheral neuritis. 
The sensory dissociation, especially in the hands and arms, is 
accompanied by atrophy and paresis. The fingers are affected 
by painless whitlows, and necrosis of the phalanges may lead 
to great deformity. 

Diagnosis. — This rests upon discovery of the loss of the pain 
and temperature senses and the preservation of tactile and 
muscular sense, in association with muscular wasting. Hyper- 
trophic pachymeningitis may resemble syringomyelia, but the 
tactile sense is usually lost, pain is greater, and the syringo- 
myelic dissociation is not present. This and other permanent 



DISEASES OF THE NERVOUS SYSTEM. 435 

cord irritations may bear an etiologic relationship to syringo- 
myelia, however. 

Prognosis. — The disease is incurable, but the course may be 
prolonged over fifteen or twenty years. 

Treatment. — This is limited to the treatment of symptoms as 
they arise. 

CAISSON DISEASE. 

(Diver's Paralysis). 

Etiology. — Persons working in caissons and diving bells under 
increased atmospheric pressure ma} 7 , on returning to the sur- 
face, be seized with pains and paralytic symptoms. The 
cause is presumably circulatory, but its exact nature is unknown. 

Symptoms. — Within half an hour after returning to the sur- 
face the patient is seized with pains in the ears and joints, diz- 
ziness, headache and nausea ; and this is suddenly followed by 
hemiplegia or paraplegia. A few become comatose and die ; 
but the majority convalesce in a few days and others in the 
course of some weeks. 

Treatment. — By allowing five minutes to each "lock," by 
means of which the air-pressure is progressively reduced, the 
disease can be avoided. Upon the appearance of symptoms 
the patient should be placed at absolute rest, and such reme- 
dies as arnica, belladonna, bryonia, causticum, mix vomica, and 
rhus tox. administered. Morpliine may be sometimes required 
for relief of the agonizing pain. 

DISEASES OF THE PERIPHERAL NERVES. 
NEURITIS. 

Etiology. — Inflammation of a peripheral nerve may be due to : 

1. Traumatism (compression, contusion, or wounds). 

2. Extension from a neighboring inflammation (arthritis, 
meningitis, etc.). 

3. Toxemia, the result of infectious diseases (diphtheria, 



436 DISEASES OF THE NERVOUS SYSTEM. 

syphilis, malaria, etc.), of poisoning from extrinsic sources 
(alcohol, arsenic, lead, mercury, etc.), or of auto-intoxication 
(diabetes, gout, etc.). 

4. Exposure to cold or dampness. 

Pathology. — The inflammation is usually confined to the nerve 
sheath or septa, but ultimately a connective tissue hyperplasia 
may ensue, which by compression destroys the nerve itself. 
Neuritis may be localized to a single nerve or area {simple 
neuritis) or widespread, involving many nerves {multiple 
neuritis). 

Symptoms. — Simple neuritis of a sensory nerve is accompanied 
by pain and tenderness along its course, together with various 
trophic changes (redness and edema of the skin, herpes, etc). 
Later, anesthesia succeeds the hypeiesthesia. Should in- 
flammation involve a motor nerve, muscular twitchings, im- 
paired motion, and paralysis are apt to result; and later 
atrophy, contractures, and the reaction of degeneration may 
supervene. 

Multiple Neuritis (polyneuritis) is always of toxic origin, and 
it involves many nerves simultaneously or in rapid succession. 
The onset may be gradual, or it may be acute and accom- 
panied by fever and febrile symptoms. The typical manifesta- 
tions vary in their relative intensity, but in some degree they 
always include : 

1. Motor weakness. The motor loss is usually more marked 
in the lower limbs ; there is foot-drop, and a characteristic gait 
in which the patient bends the thigh in order to raise the foot 
from the ground and the leg is then thrown forward like a 
flail ("steppage"). The dangling foot wears the shoe at the 
toe and frequently scrapes up the dirt of the street. In the 
upper extremities wrist-drop may be conspicuous, and in some 
cases a claw-hand. Rarely the thigh, trunk, shoulder, and 
face muscles are involved. Tremor, fibrillation, atrophy, and 
contractures may be evolved in the course of the disease. The 
reflexes are diminished or abolished, and the electrical tests 
usually show the reaction of degeneration in the diseased 
nerves. 



DISEASES OF THE NERVOUS SYSTEM. 437 

2. Sensory derangements. — As a rule the onset is attended 
by various paresthesias, such as numbness, heat, cold, etc. ; 
and varying degrees of hyperesthesia and anesthesia may also 
be present. The muscles are apt to become very sensitive as 
the disease progresses, the slightest pressure causing acute 
pain ; and the patient may suffer with crises of intense agony. 
The loss of the muscular sense sometimes leads to decided 
ataxia. 

Various trophic changes occur, especially in the skin, and 
mental symptoms, such as irritability, depression, forgetfulness, 
or delirium, are sometimes present. 

Special Forms. — The alcoJiolic form is most common ; it is 
characterized by a preponderance of sensory over motor symp- 
toms, and the latter are confined principally to the lower limbs. 
The lead palsy is usually preceded by colics and constipation, 
and the upper extremities are almost exclusively affected. 
Erythromelalgia is a variety of multiple neuritis which espe- 
cially affects the plantar nerves and is associated with burning 
pain, redness, and swelling in the feet. Beri-beri or kakke is a 
polyneuritis, possibly due to a specific organism, which is 
endemic in the Orient. 

Diagnosis. — The diagnosis of simple neuritis rests principally 
upon the localization of pain, weakness, paresthesia, and anes- 
thesia to the area supplied by a certain nerve. The diagnosis 
of multiple neuritis is rarely difficult. It may be necessary to 
exclude poliomyelitis, which is most frequent in children, 
abrupt in onset, is not usually symmetrical, has fewer sensory 
symptoms, and begins to improve almost at once but rarely 
recovers completely. Myelitis is distinguished by its girdle 
pain, paraplegia, anesthesia, and preservation of the electrical 
responses and deep reflexes. Multiple neuritis sometimes 
closely resembles locomotor ataxia and is referred to as pseudo- 
tabes. The two diseases may be distinguished by reference to 
the following table: 



438 DISEASES OF THE NERVOUS SYSTEM. 

Locomotor Ataxia, Mui/ripi,E Neuritis. 

Girdle pain, lightning pains. No girdle pains, rarely lightning 

pains. 



Nerve trunks insensitive. 



Nerve trunks tender. 



Atrophy and reaction of denenera- p re sent 
tion absent. 

Characteristic gait, due to inco-ordi- Gait due to muscular paresis, 
nation. 

Strikes heel first. Drags toe on ground, " steppage." 

No vasomotor change. Edema, discoloration, etc. 

Argyll-Robertson pupil. Absent. 

Paralysis of sphincters common. Unusual. 

Perforating ulcers, arthropathies. None. 

The discovery of the toxic cause of multiple neuritis is im- 
portant, yet often difficult. Careful investigation as to 
alcohol, lead, arsenic, diphtheria, etc., usually reveals the 
probable origin, however. 

Prognosis. — This must be governed by the intensity of the 
symptoms and the extent of degeneration revealed by the 
electrical reactions. In simple neuritis it is generally favor- 
able, although in severe cases recovery may be delayed for 
months. In multiple neuritis it is usually good, provided the 
cause can be removed. 

Treatment. — The affected area, whether a single extremity or 
the entire body, should be put at rest. The arm may be 
carried in a sling. If possible the cause must be removed. 
The diet should be very plain and non-stimulating. Hot 
applications (hot cloths, hot water bags, or the Japanese fire- 
box) serve to relieve the pain. Galvanism, a mild uninter- 
rupted current, may be used for five or ten minutes daily, and 
massage is a useful adjunct. If the pain is severe, belladonna 
is usually indicated, although in severe cases of multiple 
neuritis with burning pain arsenic is frequently preferable. 
Rhus tox. is indicated in cases due to exposure, gelsemium 
and causticum in cases presenting marked paralytic symptoms, 
and argentum nit. when ataxia is present. Cimicifuga, nux 
vomica, or strychnine may be given in alcoholic cases. 



DISEASES OF THE NERVOUS SYSTEM. 439 



NEURALGIA. 

Etiology. — Nerve pain is merely a symptom. It may be due 
to any condition which produces irritation of a nerve. The 
more important predisposing causes are: 

1. Heredity. Neuralgia is particularly common in the 
victims of neuropathic heredity. 

2. Age. It is more frequent between the thirtieth and 
fiftieth years of life. 

3. Sex. Women appear to suffer from it more often than 
men. 

4. Occupation. Painters and workers in metal are very 
liable to neuralgia. 

5. General pJiysical condition. Any impairment in health 
predisposes to neuralgia. 

Among the exciting causes are: 

1. Exposure to cold or wet. 

2. Traumatism. 

3. Irritation (thermal, chemical, or mechanical). 

4. Toxic states (gout, infectious diseases, intoxications, etc. ). 

5. Neuromata. 

Symptoms.— The characteristic neuralgic pain is unilateral, 
inconstant, and usually paroxysmal. It is described as dart- 
ing, stabbing, tearing, etc., is deep-seated, and is often accom- 
panied by cutaneous hyperesthesia. Between pains tender- 
ness can be detected at certain points where the nerve is 
superficial, overlies bone, or is inclosed by rigid tissue 
(''tender points" of Valleix). The pain may be accompanied 
by muscular spasm {e. g., tic douloureux), and occasionally 
local vasomotor symptoms (flushing, etc.), or trophic changes 
(erythema, herpes, pigmentation, etc.) may be noted. 

Varieties. — Among the more important varieties of neuralgia, 
classed according to location, are the tri-facial, cervico-occip- 
ital, cervico-brachial, dorso-intercostal, intercostal, lumbo- 



440 DISEASES OF THE NERVOUS SYSTEM. 

abdominal, spinal, sacral, sciatic, crural, metatarsalgia, etc. 
Visceral forms (e. g., gastralgia, enteralgia, etc.) are also 
noted. 

Diagnosis. — The diagnosis of neuralgia rests upon the uni- 
lateral pain, its limitation to the area supplied by certain 
nerve trunks, its paroxysmal character, and the absence of 
symptoms pointing to other conditions. In neuritis the pain 
is more constant, the functions of the nerve are interfered 
with, anesthesia and paralysis ensue, and the nerve trunk is 
more tender. 

Treatment. — Ascertain the cause, local or constitutional, and 
if possible remove it. Rest, nourishing food, and proper 
hygiene are usually prerequisites to successful treatment of the 
more chronic cases. Belladonna is useful in acute neuralgias 
of sudden onset and attended by congestive symptoms. Meze- 
reum is particularly valuable in facial neuralgias resulting from 
the irritation from decayed teeth, arsenic and cedron in neural- 
gias of malarial origin, cimicifuga and bryonia in those of 
rheumatic nature, and colcliitnn and rhus tox. in cases asso- 
ciated with a gouty state. The intense pain may often be re- 
lieved by the application of dry heat, but at times it is neces- 
sary to give acetanilid or antipyrine, gr. v-x, rarely morpliia, 
in order to relieve the suffering. In obstinate cases uncon- 
trolled by general and medicinal measures it may be advisa- 
ble to resort to stretching or resection of the nerve. 

SYPHILIS OF THE NERVOUS SYSTEM. 

Varieties. — Syphilis gives rise to an almost endless variety of 
lesions of the nervous system. These may be divided into : 

1. Lesions due to direct microbic action {specific lesions^). 

2. Lesions sequential to syphilis, not neoplastic in character, 
and due to some toxic agent {parasyphilitic lesions^). 

A systematic tabulation of the lesions (Church) follows : 



DISEASES OF THE NERVOUS SYSTEM. 



441 



Active spe- 
cific le- 



Cerebro-spinal 
syphilis, ac- 
quired and 
hereditary 
(early and 
tardy). 



Cerebral. 



Meningitis. 
! Cerebritis. 
j Arteritis. 

Neuritis. 



f Ma uia. 
j Melancho- 
i lia. 
I Pseudopa- 
L resis. 



Syphilis of 
the gen- 
eral nerv- ■{ 
ous sys- 
tem. 



Spinal. 



Meningomyelitis. 

Myelitis. 

Spinal paraplegia. 



J Syphilis of spinal nerves. 



Acquired. 



Parasyphi- 
litic Dis- 
ease. 



Hereditary. 



f Locomotor ataxia. 
| Paralytic dementia. 
J Neurasthenia, 
j Hysteria. 
| Epilepsy. 
[ Neuralgia. 

f Juvenile tabes and paresis. 
J Infantilism. 
1 Hydrocephalus. 
L Cerebral or spinal agenesis. 



Diagnosis. — Cerebral Syphilis presents some features which 
are so characteristic that even without a history of previous 
infection the diagnosis is not difficult. The development of 
brain-syphilis is apt to be marked by a series of advances, each 
followed by a partial remission ; it is almost never abrupt in 
onset. Nocturnal headache, often atrociously severe, and fre- 
quently associated with cranial nerve symptoms (diplopia, 
ptosis, pupillary changes, optic nerve disturbances) is well-nigh 
pathognomonic. Epileptoid attacks appearing after the thir- 
tieth year of life, and apoplectiform seizures occurring before 
the age of fifty, afford strong presumptive evidence of syphilis. 
A multiplicity of lesions, e. g., brain and cord symptoms in the 
same patient, should arouse suspicion. Finally, the therapeutic 
test (large doses of the iodides), if followed by improvement 
within a week, strongly sustains the diagnosis of syphilis. It 
must not be forgotten, however, that the symptoms of other 
organic brain diseases, even those due to a neoplasm, may be 
somewhat ameliorated by the administration of iodides. 

Spinal Syphilis affords far greater diagnostic difficulty. It 
has no characteristic premonitory symptoms, and its distinc- 
tion must often rest upon a history of infection or upon asso- 
ciated cerebral symptoms of a suggestive sort. The irregular 
advance and retreat of the symptoms is somewhat significant. 

Prognosis. — -The prognosis of cerebro-spinal syphilis is by no 
means as favorable as is popularly supposed, less than one- 



442 DISEASES OF THE NERVOUS SYSTEM. 

fourth of the cases recovering completely. This is, of course,, 
because of the disintegration and destruction of the tissues 
secondary to the specific lesion; and consequently early dis- 
covery and energetic treatment of the latter becomes doubly 
imperative. 

Treatment. — Administer at first twenty drops of a saturated 
watery solution of sodium iodide in a glassful of water or milk 
three times a day, after meals. Increase this dose by ten 
drops daily until, in critical cases, 100 or even 200 drops are 
given at a dose. In the meantime it is often advisable to give 
mercury by inunction; 3ss-3j of the ointment should be applied 
daily to different parts of the body, as directed in the general 
treatment of syphilis (page 108). Aftera week or two omit the 
mercury and continue the iodide alone for a week; then stop 
the latter, and return to the mercurial inunctions for a week; 
and so continue to alternate the remedies. The dose should 
be decreased as the symptoms yield, but must be continued 
for six months; and for five years thereafter the patient should 
undergo an annual course of six months' specific treatment. 



THE NEUROSES. 

(Functional Nervous Diseases, i. e , Diseases of Undetermined Patho- 
genesis.) 

HYSTERIA. 

Etiology. — Hysteria is a psychoneurosis the exact nature of 
which remains undetermined, but its manifestations are un- 
doubtedly due to the control of the body by ideas. Among 
the important predisposing factors are: 

1. Sex. A decided majority of hysterical patients are 
females. 

2. Heredity. A hereditary neurotic taint is the most potent 
factor in the production of hysteria. Other neuroses and 
diatheses, notably gout and tuberculosis, are important ante- 
cedents of hysteria, as of other forms of degeneracy. 



DISEASES OF THE NERVOUS SYSTEM. 443 

3. Age. The period of puberty and adolescence furnishes a 
majority of the cases of hysteria. As life advances the fre- 
quency of the disease lessens, and after the age of 45 it is rare. 

The exciting cause of the hysterical manifestations is almost 
invariably an emotional disturbance, due to mental or moral 
strain (overwork, worry, grief, etc.), or to shock, either 
psychical or physical (fright, traumatism). The disease may 
become epidemic in small, closely-associated communities, 
such as schools, nurseries, and remote villages, as the result 
of imitation, a so-called " moral contagion." 

Symptoms. — The manifestations of hysteria are divisable into 
two groups, one of which is persistent so long as the disease 
lasts — the stigmata; and a second group consisting of S3 r mp- 
toms which appear incidentally and are often transitory — the 
paroxysmal phenomena. 

A. Stigmata. 1. Sensory stigmata. These disorders may 
be negative, i. e., anesthesia, or positive, i. e., hyperesthesia. 

Hysterical anesthesia may affect sensation in all its varieties 
and distributions. Cutaneous insensibility may be so absolute 
that neither pinching, pricking, nor the application of hot or 
cold substances to the skin elicits the slightest response; and 
the mucous membranes of the mouth and throat and other 
orifices are often equally insensitive. The deeper tissues are 
also frequently anesthetic, so that muscles, ligaments, and 
nerve trunks may be twisted or pierced without evoking the 
slightest sensation. The muscular sense may be so completely 
abolished that the patient when blind-folded has no knowl- 
edge of the position of a limb, nor can she recognize pressure 
or fatigue. 

The special senses may be equally affected. Smell and 
taste may be perverted, diminished, or abolished, the acuity of 
hearing may be lessened, and vision may be modified or 
abolished. More commonly the visual disturbance consists 
of— 

(a) Contraction of the visual field. This is usually con- 
centric and often bilateral. 



444 DISEASES OF THE NERVOUS SYSTEM. 

(b) Difficulty in color perception (dyschromatopsia) . In 
health blue has the largest field, followed by yellow, orange, 
red, green, and violet. In hysteria, and also in neurasthenia, 
these fields may be contracted, and, more important, their 
order is changed, the red field exceeding the blue; and should 
the color fields become extinguished, red is the last to disap- 
pear. All objects then appear grayish in color {achromatop- 
sia). 

(c) Errors of accommodation. Near vision may be rendered 
faulty, or monocular diplopia, macropsia, or micropsia may 
be present. The patient mav aver that she sees nothing 
with one eye, yet perceives two images when a prism is placed 
before either eye, indicating that she sees without knowing it. 
A characteristic symptom is "crossed amblyopia," one eye, 
particularly that on the side which is paralyzed or anesthetic, 
seeing poorly, while the other is less affected. 

The distribution of hysterical anesthesia is characteristic. 
Rarely the entire skin and membranes are affected ; as a rule 
it is : 

(1) Limited to one-half the body, especially the left (hys- 
terical hemianesthesia). 

(2) To definite areas, usually about an extremity on which 
may be outlined the position of a sleeve, glove, sock, or stock- 
ing. In any case the outlines have no relation to the area of 
distribution of the nerve trunks. 

(3) Discrete islets of anesthesia may be present, minute 
search being necessary for their discovery. 

The peculiarities of hysterical anesthesia are : 

(a) The area does not conform to the distribution of the 
cutaneous nerves or to the spinal segments. 

(b) The pupillary and tendon reflexes are not modified as in 
organic lesions. 

(c) The areas are movable, enlarging, shifting, or at times 
disappearing. 

(d) The patient is usually ignorant of the existence of these 
anesthetic areas. 



DISEASES OF THE NERVOUS SYSTEM. 445 

Hysterical hyperesthesia is common. There may be a fixed 
boring pain in one spot, usually the temple (clavus), or there 
may be pain in the back, the breasts, in the pit of the stomach, 
or in certain joints. Tenderness is even more common. If 
such a hyperesthetic area has been associated with some mental 
storm, pressure upon it, by reviving the memory, may provoke 
a hysterical seizure (hysterogenic zone). 

2. Motor. Stigmata. These stigmata must be carefully 
distinguished from the paroxysmal motor phenomena. They 
consist simply of slight retardation, inco-ordination, or weak- 
ness of intentional movements, together with a tendency to 
rigidities or contractures. 

3. Mental Stigmata. These stigmata consist of: 

(a) Amnesia (loss of memory), the patient's lack of mental 
concentration leading to forgetfulness and consequently un- 
certain and contradictory statements, or to the loss of certain 
motor images, such as those for walking, writing, or speech, 
with astasia, agraphia, or motor aphasia as a result. Occa- 
sionally the patient loses the memory of a certain period of 
time, and out of this a double personality may arise, the 
patient alternately recognizing one group of memories and 
then the other. 

(b) Abonlia (absence of will power) is constant in hysteria. 
As a result the patient, is vacillating, impulsive, impression- 
able, and lacking in determination. 

B. Paroxysmal Phenomena. 1. Convulsive attacks. 

(a) Hysteria major. The severe, intense, and prolonged 
convulsive seizure {grand mal hysterique) described by 
Charcot is rare in this county. Such a paroxysm consists of 
a premonitory stage, in which various emotional and psychic 
disturbances may be present, followed by an aura (frequently 
the globus hystericus), and then an epileptoid seizure which 
closely mimics the true epileptic convulsion, and lasts about 
three minutes. At the close of this a period of clownism 
appears, the patient going through various contortions and 
wider-ranged movements. During this stage the patient 



446 DISEASES OF THE NERVOUS SYSTEM. 

often utters violent outcries, grimacing, and biting, scratching, 
or striking at her attendants. The seizure may terminate in 
a period of passional attitudes, in which the patient depicts in 
pantomime love, rage, gaiety, or terror, or a period of delirium 
may supervene, the patient verbally expressing the hallucina- 
tions previously evidenced in pantomime. Finally, either sud- 
denly or after a short period of silence, she arouses to her usual 
conscious state. The entire attack may consume from fifteen 
minutes to half an hour. 

(&) Hysteria minor. Modified or partial seizures are fre- 
quently encountered. The more usual of these are attacks of 
vertigo, globus, epileptoid paroxysms, tetanic seizures, syn- 
cope, lethargy or trance, and somnambulism. 

2. Motor Phenomena. Paralyses or contractures of a hys- 
terical nature may follow convulsive seizures, shock, trauma- 
tism, or various morbid states. The paralyses often develop, 
either abruptly or gradually, after an emotional disturbance, 
but rarely is every movement of the extremity completely abol- 
ished. Antagonistic muscle groups are affected and the limb 
is perfectly limp ; while the electrical reaction and reflexes are 
normal. Anesthesia or hyperesthesia may be associated. Hys- 
terical contractures are characterized by loss of power and per- 
sistent involuntary rigidity, without change in the electrical or 
tendon responses. Among the most typical of hysterical motor 
phenomena are : 

Hysterical hemiplegia, more frequent on the left side, and 
usually incomplete ; often it affects only the distal portion of 
the limb. Instead of the rigidity of organic hemiplegia, the 
limb is flaccid ; for example, in walking the leg is simply drag- 
ged along the ground. 

Hysterical monoplegias may be single or multiple, unilateral 
or crossed. As a rule the member is overlaid by an area of 
anesthesia of greater extent than the paralysis. 

Astasia-abasia is a hysterical condition in which coordina- 
tion of the movements necessary for walking or standing is 
abolished. While in a bed or chair the patient has complete 



DISEASES OF THE NERVOUS SYSTEM. 447 

control of her limbs, but is unable to stand, or, if standing, to 
walk. She may at the same time be able to run, leap, or hop. 
The condition is due to a form of amnesia, the motor image of 
walking being lost. 

Hysterical rythmical spasms may be exemplified in periods 
of nodding, sneezing, grunting, or choreiform movements. 
Hysterical tremors may be of any variety, even the intentional 
form ; and hysterical tics, movements of a purposive charac- 
ter, are sometimes seen. 

3. Sensory Phenomena. The hysterical patient may suf- 
fer with persistent headache, spinal sensitiveness, visceral 
neuralgias, or even pseudo-angina pectoris. The resemblance 
of these disturbances to corresponding symptoms of organic 
disease is often close. 

4. Visceral Phenomena. In hysteria the respiratory tract 
may be affected, stammering, coughing, dyspnea, and aphonia 
being sometimes induced. The last-named symptom is fre- 
quently due to a hysterical paralysis of the larynx. 

The digestive system is usually involved, the symptoms vary- 
ing from anorexia to esophageal spasm, and attacks of hys- 
terical vomiting. Various abdominal disturbances may also be 
present, and in connection with contracture of the muscles a 
phantom tumor may be produced. Constipation is very com- 
mon. Urinary disturbances, varying from anuria to the dis- 
charge, often after a hysterical crisis, of large quantities of 
limpid urine, may occur. Many hysterics are troubled with 
frequent urination. Even fever, may, though rarely, be of 
hysterical origin. 

5. Trophic and Vasomotor Phenomena. These are few in 
number and quite rare ; they consist of erythematous or vesic- 
ular eruptions, and local asphyxias similar to those of Ray- 
naud's disease. 

Diagnosis. — -The diagnosis of hysteria must be based upon the 
complete exclusion of all possible organic causes for the phe- 
nomena present. The disease should be sharply distinguished 
from neurasthenia, simple emotional disturbances, and malin- 



448 DISEASES OF THE NERVOUS SYSTEM. 

gering. The mental and psychic characteristics are often in 
themselves distinctive. In every case search should be made 
for the sensory stigmata ; the disturbance of the color fields, 
and the peculiar outlines of anesthesia, with movability of the 
anesthetic areas, are practically pathognomonic. It must be 
remembered, however, that hysteria can coexist with organic 
disease, and in consequence such affections as tuberculosis, 
chronic nephritis, and cerebral hemorrhage must not be over- 
looked because of their development in a patient hitherto 
neurotic. 

Prognosis. — Hysteria is essentially dependent upon a mental 
state, a temperament rather than a disease, and in conse- 
quence it cannot be wholly eradicated. Its paroxysmal phe- 
nomena are often controllable, however, particularly when in- 
fluenced by certain mental and moral suggestions. 

Treatment. — Since hysteria rests upon a mental basis, the 
treatment must be principally psychic. The physician must 
secure for himself and his measures the absolute confidence of 
the patient; and on this account the use of novel methods 
calculated to strike the fancy of the sufferer and inspire hope- 
fulness is fully justified. In short, the treatment must be 
suggestive. 

In order to accomplish this the patient should be isolated, 
and thus cut off from the friends and surroundings associated 
with the morbid past. The environment must be cheerful, and 
the attendants sensibly but not solicitously sympathetic, and 
at the same time optimistic. In severe cases these conditions 
are best secured by the rest cure in charge of a suitable nurse. 
In milder cases and in the young a prolonged journey with a 
sensible companion may meet all requirements. Medicines 
are of only secondary importance, but general conditions may 
afford indications for the administration of such remedies as 
belladonna, cimicifnga, ignatia, mix vomica, Pulsatilla, and 
many others. 

Special symptoms may be met by special measures. A con- 
vulsion may be checked by a sharp command, a dash of cold 



DISEASES OF THE NERVOUS SYSTEM. 449 

water, or by pressure upon a hysterogenic zone. Paralyses 
and contractures, while often intractable, may be overcome if 
treated early by massage, electricity, and repeated suggestions 
of cure. Anesthesia and hyperesthesia may be abolished or 
modified by the use of faradism. Aphonia also may be over- 
come by the local application of faradism, coupled with ma- 
nipulations and verbal suggestions of recovery. Dysphagia 
may be controlled by passing a stomach tube and thus prov- 
ing that the esophagus is not obstructed. 

EPILEPSY. 

Etiology. — Epilepsy is in reality a generic term for a group of 
symptoms due to various pathological conditions. Among the 
more important predisposing causes are: 

1. Heredity. A neurotic ancestry is an important factor in 
the production of epilepsy. Frequently the latter represents 
a transformation from other ancestral neuroses (hysteria, in- 
sanity) or from arthritis, syphilis, or alcoholism. 

2. Age. It is uncommon for epilepsy to begin after the age 
of thirty, and a majority of the cases originate within the first 
twenty years of life. Epileptoid attacks occurring later in 
life should arouse a suspicion of syphilis, gross brain lesions, 
degenerative changes, or traumatism. 

The exciting causes may be fright, toxic agents (especially 
alcohol), infectious diseases (exanthemata), head injuries, and 
reflex irritations (intestinal worms, pelvic diseases, nasal 
growths, eye strain, etc.). 

Pathology. — While not yet clearly understood, epilepsy is 
unquestionably a disease of the cerebral cortex. 

Symptoms. — Epilepsy may be characterized by convulsions 
more or less typical, by certain post-epileptic states, and by 
mental and physical degeneration. 

1. Epileptic convulsions. The typical epileptic attack (grand 
vial) may be preceded by slight temperamental changes, mild 
motor or sensory disturbances, or other vague prodromes. 
29 



450 DISEASES OF THE NERVOUS SYSTEM. 

The attack is ushered in by an aura which may be motor 
(muscular contraction, tremor, automatic movement, etc.), 
sensory, a peculiar sensation arising in the abdomen or ex- 
tremities and mounting to the head, or involving a special 
sense (visual or auditory sensations, etc.), or psychic (gaiety, 
rage, etc). This is immediately followed by a convulsion 
which presents three distinct periods : (1) A tonic stage, the 
patient uttering a cry and falling in a state of tetanic rigidity 
which lasts but a minute or two, and is followed by : (2) A 
clonic stage, in which the muscles alternately relax and con- 
tract, thus causing a horrible twitching which usually involves 
the entire body- This continues for from one to five minutes, 
when it is succeeded by : (3) A stage of stertor, in which the 
convulsive movements cease and the patient lies comatose and 
breathes stertorously. After a few minutes, perhaps half an 
hour or more, he gradually regains consciousness but has no 
knowledge of what has happened. During the convulsive 
period, the tongue maybe bitten and the contents of the bowel 
and rectum expelled. 

Modifications of this typical fit are not uncommon; the 
clonic movements may be confined to one extremity, or to 
one side of the body, or the cry, stertor, or urination may be 
lacking. In some cases the attacks occur only during sleep 
(nocturnal epilepsy), and thus the disease may exist unsus- 
pected for years. Occasionally the patient has a series of fits 
one after the other without recovering consciousness (status 
epilepticus). 

2. Incomplete attacks (petit vial). Almost any part of the 
attack may occur alone; for instance, the patient may be 
seized only with an aura, or with vertigo, or with a momen- 
tary loss of consciousness. In rare instances the patient is 
seized with an irresistible impulse to walk or run, and 
this latter phenomenon sometimes immediately precedes or 
follows a typical convulsion. Certain psychic phenomena, 
automatic actions of a homicidal or obscene character, may 
appear in place of or in alternation with the typical attack 
{psychical epilepsy). The physical condition of the average 



DISEASES OF THE NERVOUS SYSTEM. 451 

epileptic is good, except for the gastro-intestinal and other 
disturbances induced by the bromides or similar drugs with 
which he has been dosed; but his mental state undergoes pro- 
gressive deterioration. 

Diagnosis. — As a rule the typical attacks offer no diagnostic 
problem, but incomplete seizures may be extremely difficult of 
recognition. Suspicion should be aroused by a history of bed- 
wetting, unexplained bruises or ecchymoses, a bitten tongue, 
etc., and in such a case attacks of momentary unconsciousness 
or of sensory aura are extremely significant. Repeated con- 
vulsions of epileptic type are rarely mistaken for anything 
else. Organic brain disease may produce epileptoid convul- 
sions, but such cases are distinguished by a history of head- 
ache, pain, vomiting, vertigo, optic neuritis, and other symp- 
toms of cerebral disease. As a rule, the patient is older, the 
attacks are more protracted than those of epilepsy, conscious- 
ness may not be entirely lost, and sometimes the convulsion is 
Jacksonian in type and is followed by paralysis of the pre- 
viously convulsed parts. Uremic convulsions closely resemble 
those of epilepsy, but as a rule they occur in later life, the 
seizures are prolonged, and the urine is apt to contain albumin, 
casts, and a deficient amount of urea. 

For the differentiation of hysterical and epileptic seizures, 
the following table (Church) may be consulted: 

Epilepsy. Hysteria. 

Prodromes. Mental or physical premoni- Emotional disturbance, 
tions. 

Aura. Common but momentary. Uncommon and of considerable 

duration. 
Onset. Sudden, complete; cry, fall, Gradual, 

rigidity. 

Conscious- Instantly lost. Partially lost or retained, 

ness. 

Course. Tonic, clonic, and stertorous Epileptoid and emotional 

stages. phases. 

Duration. Two to five minutes. A few minutes to several hours. 



452 



DISEASES OF THE NERVOUS SYSTEM. 





Epilepsy 




Hysteria. 




Positions. 


Governed by flexors mainly. 


Tendency to extension, 
circle, opisthotonos, 
fixion attitude, etc. 


arc de 
cruci- 


Eyes. 


Pupils dilated and rigid. 




Pupils mobile and active. 




Tongue. 


Usually bitten. 




Bitten very exceptionally 




Mouth. 


Frothing common. 




Absent. 




Sphincters. 


Relaxed usually. 




Usually continent. 




Pulse 


Accelerated greatly and 
sion increased. 


ten- 


Rate and tension not 
changed. 


much 


Tempera- 
ture. 


Elevated i° or 2° F. 




Normal. 





Post-parox- Petechial ecchymoses, re- No motor or reflex changes; 

ysmal con- duced muscular strength, some recollection of phases of 

ditions. diminished knee-jerks, attack; usual mental condi- 

mental obscuration, no tion at once regained; pres- 

memory of attack. ence of various stigmata. 

Prognosis. — -Recovery is rare, and after the disease has be- 
come thoroughly established there is scarcely any hope of cure. 
Death may occur in a status epilepticus, or as a result of injury 
received during a convulsion. Otherwise, the natural termi- 
nation of the disease is in dementia. 

Treatment.— Study the patient thoroughly. Remove every 
possible source of reflex irritation, correcting eye strain, nasal 
disease, and dental, gastro-intestinal, and genital troubles. 
Regulate the diet so that it is nourishing and. digestible ; allow 
vegetables, fresh fruit, milk, and fish, a limited amount of 
starchy food, and little meat. Direct the patient to bathe 
daily, to live a vigorous out-door life as far as possible, and in 
other respects regulate his hygiene. The more important 
medicines are argentumnit. } belladonna, bryonia, calcareacarb. 
cicuta, cuprum, hydrocyanic acid, hyoscyamus, mix vomica, 
cenantJie, plumbum, Pulsatilla, and sulphur. Only as a last 
resort, these having failed, is it justifiable to resort to the 
bromides of potassium, sodium, or strontium; of these, from 
fifteen to thirty grains may be given daily in divided doses, 
each of the latter being dissolved in a large quantity of water 
aud taken after meals. 



DISEASES OF THE NERVOUS SYSTEM. 453 



NEURASTHENIA. 

(Nervous Prostration ; Nervous Exhaustion). 

Etiology. — Neurasthenia is a condition of ''irritable weak- 
ness," a neurosis in which all forms of nervous energy — 
psychic, motor, and organic — are reduced, as a result of fatigue 
of the nerve cells. The more important predisposing causes 
are : 

1. Age. The condition seldom develops before the twentieth 
or after the fiftieth year of life ; it is a disease of the energetic 
period. 

2. Heredity. While neuropathic antecedents are less com- 
mon than in hysteria or epilepsy, nevertheless debilities in the 
parents are apt to weaken the offspring and so lessen the en- 
durance of the latter. 

The exciting cause of neurasthenia is usually overwork, often 
associated with worry and excitement, alcoholic or sexual ex- 
cesses, exhausting illness, and such toxic states as gout or 
syphilis. Shock, either traumatic or psychic, may be a direct 
cause. 

Symptoms. — The general depression of nervous energy gives 
rise to a host of symptoms, the more important of which may 
be classified under the following heads, viz. : 

1. Motor disorders. — Muscular weakness is a constant com- 
plaint, the patient becoming fatigued on the slightest exer- 
tion. Tremors and muscular twitching are common, and the 
tendon reflexes are increased. 

2. Sensory disturbances. — The patient feels generally tired 
and fatigued. He complains of headache, often at the base of 
the brain, and at other times of a terrible weight, like a lead 
cap, over the head. Backache is equally common. Tender- 
ness over the spine is usually present, but cutaneous anesthe- 
sia, never. Many vague subjective sensations, such as numb- 
ness, prickling, soreness, etc, are encountered. 



454 DISEASES OF THE NERVOUS SYSTEM. 

3. Gastro-intestinal disturbances. — Nervous dyspepsia, with 
the various symptoms and signs peculiar to that disorder, is 
characteristic of neurasthenia. Constipation, due to atony of 
the intestines, is also common. 

4. Circulatory disorders. — These patients frequently suffer 
with palpitation, and even with attacks of pseudo-angina. 
Often the circulation is feeble, the pulse rapid and the extremi- 
ities cold, and vasomotor symptoms, such as flushes and sweats, 
occur. The fluid secretions may be scanty. The hand is usu- 
ally cold and clammy with perspiration. 

5. Disorders of special sense. Reading causes headache 
and distress, the accommodative apparatus and the retinal 
sensibility becoming quickly fatigued. Photophobia and 
hypersensitiveness to sounds, smells, and tastes are common 
symptoms. 

6. Genital disorders. The male neurasthenic usually com- 
plains of lessened sexual power, or he may be frightened by 
nocturnal emissions. If he has at any time masturbated, his 
time is spent brooding over that and its supposed effects, 
especially his impotency {sexual neurasthenia). 

7. Mental disturbances. The capacity for mental work is 
reduced, the memory is poor, and as a result the patient be- 
comes introspective and hypochondriacal. Morbid fears and 
emotional outbreaks are common, while insomnia is almost 
habitually present. 

Diagnosis. — The diagnosis of neurasthenia is generally easy, 
b"t it must be remembered that the condition is frequently 
merely symptomatic of some organic process, e. g. } following 
any exhausting illness or accompanying anemic or cachectic 
states. It is frequently associated with Jiysteria, and so closely 
may the two resemble each other that it is only by discovery 
of the hysterical stigmata that the distinction can be made. 
Hypochondriasis is in reality a melancholia, the patient suffer- 
ing with delusions concerning his bodily state. 

Prognosis. — Neurasthenia is essentially a chronic disease, in- 
sidious in its onset and tending, if untreated, to persist indefi- 



DISEASES OF THE NERVOUS SYSTEM. 455 

nitely. If proper treatment, i. e., protracted rest and change, 
can be secured, the outlook is usually favorably. Relapses are 
common, however. 

Treatment. — 1. Rest. This constitutes the one essential 
factor for successful treatment. According to the severity of 
the malady and the temperament of the patient, this rest may 
be partial, the patient retiring immediately after the evening 
meal and sleeping late in the morning, or complete, the 
patient being placed at absolute rest under the care of a nurse 
for a period of several weeks. In every case the amount of 
work must be reduced, and frequently this is best accomplished 
by sending the patient on a vacation which entails prolonged 
separation from business and provides a maximum of fresh air 
and recreation without undue physical exertion. For this pur- 
pose a sea voyage is admirable. 

2. Diet. A nourishing, non-stimulating diet which tends to 
fatten the patient should be insisted upon. It matters not 
what he eats, provided enough is taken and digested. A glass 
of hot milk or beer at bed time encourages sleep. 

3. Hydrotherapy. A warm bath of five or ten minutes' dura- 
tion should be taken immediately before retiring. A cold 
spinal douche or a quick cold sponging on arising is invigorat- 
ing. 

4. Massage is essential when the complete rest treatment is 
carried out; in other cases it is not so necessary, but unques- 
tionably aids the nutritional progress. 

5. Environment. On account of the mental element present 
in neurasthenia, the patient's surroundings should be cheerful 
and his attendants should offer constant hope and encourage- 
ment. The physician should see him frequently, explaining 
away his fears, but refusing tactfully to let him reiterate his 
complaints. 

6. Medicines. — Among the many useful remedies are argen- 
tum nit., cimicifuga, mix vomica, phosphorus, phosphoric acid; 
picric acid, platina, sepia, strychnine, sulphur and zinc. 



456 DISEASES OF THE NERVOUS SYSTEM. 

CHOREA. 

(Chorea Minor; Sydenham's Chorea.) 

Etiology. — Chorea must be carefully distinguished from other 
choreiform affections, such as habit chorea, hereditary chorea, 
the various forms of tic and myoclonus, and the hysterical 
manifestation properly known as St. Vitus's dance. The more 
important predisposing factors are: 

1. Sex. Girls are affected much more frequently than boys. 

2. Age. The great majority of cases develop between the 
fifth and fifteenth years of life. 

3. Heredity. The neurotic heredity plays an important 
part in the production of this, as of the other neuroses. 

4. Season. Chorea is most frequent in the winter and spring" 
months, thus corresponding to rheumatism and other diseases, 
whose prevalence is affected by climatic vicissitudes. 

Among the exciting causes have been listed fright, worry, 
shock, overwork, and reflex irritation from the intestines. This, 
relationship is in all probability simply coincidental, for the 
trend of modern investigation is to demonstrate that chorea,, 
which is so commonly associated with more or less typical 
rheumatic manifestations, is due to a similar infective agent. 

Pathology. — The disease is probably localized in the cerebral 
cortex, although no distinctive lesions have been demon- 
strated. In fatal cases the heart lesions characteristic of rheu- 
matism (endocarditis, pericarditis) are usually discovered, 

Symptoms. — The disease develops insidiously, the child first 
becoming peevish, inattentive, and depressed. This is fol- 
lowed after a varying period by — 

1. Choreic movements. These are sudden, involuntary, 
slight movements which make the child appear maladroit, up- 
setting his cup, dropping things from his hand, etc. Twitch- 
ing of the facial muscles causes various grimaces, and the 
involvement of the muscles of the tongue may render speech 
indistinct and swallowing difficult. Station may be unsteady 



DISEASES OF THE NERVOUS SYSTEM. 457 

and the gait irregular because of the twitching of the muscles 
of the lower limbs. Involvement of the thoracic muscles and 
diaphragm may cause irregular breathing and sometimes spas- 
modic noises. Muscular power is always decreased, and in 
many cases this amounts to an actual muscular paresis. 

2. Mental disturbances. Mental activity is lessened, the 
patient is forgetful, and often the face appears inane and 
stupid. Visual hallucinations may be present, particularly at 
night; and in the grave form elevation of temperature may 
be accompanied by delirium. 

3. Cardiac disorders. Cardiac murmurs, both functional and 
organic, are extremely common in choreic patients. Endo- 
carditis, sometimes associated with joint symptoms, occurs in 
more than half of the cases; and the resulting valvular lesions, 
of which mitral insufficiency is the more frequent, persist 
throughout life. 

Forms. — In addition to the ordinary variety just described, 
three others may be distinguished, viz. : 

The grave form, {chorea gravis) is acute in its onset, marked 
by severe mental and motor phenomena, and accompanied 
by fever and delirium {choreic status). This persists for days 
and frequently terminates in coma and death. 

The chorea of pregnancy (chorea gravidarum) appears espec- 
ially in young primiparse, presents intense motor agita- 
tion, and usually persists until the uterus is emptied. It is 
often fatal (20%), or it may recur with subsequent pregnancies. 

Paralytic chorea is characterized by the predominance of 
muscular paresis. It may be monoplegic, hemiplegic, or para- 
plegic in its distribution. The muscles are toneless, and the 
reflexes are abolished, but the reaction of degeneration is 
absent, and recovery within a few weeks is the rule. 

Diagnosis. — The symptoms usually facilitate a diagnosis, but 
it is necessary to distinguish chorea from the other diseases 
presenting choreiform movements. A thetosis, post-hemiplegic 
chorea, and Friedreich 's ataxia may be recognized by their 
cerebral associations. Huntingdon s chorea has a history of 



458 DISEASES OF THE NERVOUS SYSTEM. 

heredity, appears in adults, and is accompanied by progessive 
dementia. The various tics are more sudden and are ges- 
ticulatory in character. 

Prognosis. — As a rule, chorea gradually declines, and in the 
course of from one to four months terminates in recovery. 
Recurrences are very common, however, and the possibility 
of serious cardiac complications must also be remembered. 
The grave form is usually fatal, and the chorea of pregnancy 
often proves fatal to the mother, and yet more frequently 
destroys the fetus. 

Treatment. — 1. Rest. As a rule the child should be kept at 
home and away from violent romping or excitement. The 
hours of sleep should be prolonged, and frequent sponge baths 
and warm general baths and gentle massage are helpful. The 
more important medicines are agaricin, actea, belladonna, 
causticum, cuprum, ferritin, hyoscyamus, iodine, mygale, nux 
vomica, Pulsatilla, stramonium, tarantula, and zinc. 

The severe cases require absolute rest in bed, forced feed- 
ing is often advisable, and hot baths or cold packs should be 
used to meet the same indications as in any infectious fever. 
In extreme cases it may be necessary to resort to chloral, 
bromides, or even morphia. In the chorea of pregnancy, 
violent motor manifestations sometimes, though rarely, render 
render it necessary to terminate gestation, 



TETANY. 

(Tetanella. ) 

Etiology. — This peculiar tonic spasm of bilateral groups of 
muscles is rare in America, but quite common in continental 
cities. It appears usually before the twentieth, always before 
the fiftieth year of life. The principal predisposing factor is 
impaired nutrition, due to gastro-intestinal diseases, infections, 
pregnancy, myxedema, etc. The attack may be precipitated 
by exposure, exhaustion, or emotional disturbance, although 
the existence of an infective organism is suspected. 



DISEASES OF THE NERVOUS SYSTEM. 459 

Symptoms. — The attacks are initiated by a sensation of numb- 
ness and prickling in the fingers or toes, followed by a tonic 
spasm affecting chiefly the flexor muscles of both arms and 
both legs. The attacks may last for minutes or hours, seldom 
days. Several paroxysms usually occur daily. Intervals of 
days, weeks, or months may separate the seizures, but the 
latter can be provoked at any time by pressure over the larger 
nerve trunks and arteries of the arm ( Trousseau' 's phenom- 
enon). A facial spasm, limited to the distribution of the nerve 
or branch pressed upon, can be aroused in similar fashion 
(Chvostek's sign). Electric irritability, especially to the gal- 
vanic current, is exalted (Erb's phenomenon) . The temperature 
is usually normal, and cutaneous sensibility and the reflexes 
are unaffected. 

Diagnosis. — The characteristic spasms, accompanied by me- 
chanical and electrical over-excitability of the nerves, render a 
mistake improbable. Tetanus begins with masticatory stiff- 
ness, which does not subside in the intervals between spasms; 
the disease begins in the trunk, frequently sparing the hands; 
and the peculiar phenomena of tetany are absent. Hysteria 
also lacks the latter signs and presents its own peculiar stig- 
mata. 

Prognosis. — The disease usually runs a mild course, recovery 
ensuing in a few weeks; but in some cases in which the cause 
of the underlying malnutrition is not removable (e. g., dilata- 
tion of the stomach) it may be protracted or even produce 
death by asphyxia. In connection with myxedema strumipriva 
it is very fatal (80%). In other cases it tends to recur. 

Treatment. — The treatment should be directed to the cause 
of the underlying malnutrition. Quiet, rest and warm baths 
aid in controlling the attacks. Belladonna, magnesia phos. , 
mix vomica, and secale have been recommended, but in general 
remedies should be prescribed for the causative condition. 

CHOREIFORM DISEASES. 

Huntingdon's (Hereditary) Chorea appears in adult life, between 
the ages of thirty and fifty, as a result of direct heredity. The 



460 DISEASES OF THE NERVOUS SYSTEM. 

twitchings begin gradually in the upper half of the body, in- 
creasing in distribution and intensity. The disease is accom- 
panied by a progressive mental impairment which terminates, 
in dementia. The affection is chronic and incurable, and its 
pathology is unknown. 

Habit Chorea (Habit spasm) is a condition presenting definite 
spasmodic movements, such as blinking the eyes, twitching 
the nose or the corners of the mouth, or shrugging the should- 
ers. In children the prospect of recovery from the habit is 
good, but should the disease persist into adult life it is not so 
promising. 

Electrical Chorea (Dublin s disease) is a very rare affection 
which occurs in certain districts in Italy. It is characterized 
by sharp spasmodic muscular movements, similar to those 
produced by electrical discharges, which involve each of the 
extremities in succession. The muscles become weak and un- 
dergo atrophy, general paralysis ensues, and the patient dies. 

Myoclonus (Paramyoclonus multiplex) is a term comprehend- 
ing a group of diseases characterized by involuntary, sharp 
contractions of a muscle or group of muscles, similar to those 
produced by an electric shock. They are usually bilateral in 
character and arhythmic. They involve first the lower limbs 
then the upper, but are apt to spare the face. The course ex- 
tends over months, but recovery generally occurs. Tics are 
to be distinguished; they are usually at first unilateral, affect 
the face, and are purposive, expressive, or gesticulatory in 
character. 

PARALYSIS AGITANS. 

(Parkinson's Disease; Shaking Palsy.) 

Etiology. — The factors predisposing to paralysis agitans are 
age (40-70 years), sex (two-thirds of the patients are males), 
and a neuropathic heredity. Fear, anxiety, grief, exhaustion, 
shock and traumatism have been named as exciting causes. 

Pathology. — While the disease is classed as a neurosis, it is 
probable that vascular changes in the peduncular circulation,, 
leading to degenerative processes, underlie the disease. 



DISEASES OF THE NERVOUS SYSTEM. 461 

Symptoms. — The disease begins with rigidity in one arm and 
tremor of the fingers; and these symptoms extend first to the 
foot of the same side, then to the hand and foot of the 
opposite side. Ultimately there is stiffness of the whole 
body. The symptoms in a typical case are very striking; they 
include: 

1. Muscular rigidity. The attitude of the patient is char- 
acteristic: his head and body are bent forward, his neck is ex- 
tended, and he walks or trots with short, shuffling steps as 
though following his centre of gravity {propulsion) . His elbows 
are flexed and slightly abducted, bringing his hands to the level 
of the groins. The rigidity may impede passive motion, but 
the reflexes are only slightly increased and clonus never 
develops. The stiffness of the muscles renders the face immo- 
bile and mask-like; and speech is monotonous and deliberate. 

2. Tremor. The tremor may appear with or after the rigid- 
it}*. The patient appears to be rolling a pill between his 
fingers and thumb. The tremor affects all the extremities, but 
seldom involves the head muscles. It continues when the 
member is at rest, but ceases upon voluntary motion, and dur- 
ing sleep. The tremor makes itself apparent in the hand- 
writing. 

Diagnosis.— Typical cases are diagnosed at a glance. In 
senile tremor the head is first affected, rigidity is lacking, and 
the patient is advanced in years. Disseminated sclerosis pre- 
sents an "intention" tremor, increased reflexes, scanning- 
speech, and nystagmus. A post-Jiemiplegic tremor has a his- 
tory of a stroke, together with unilateral paralysis and increased 
reflexes. 

Prognosis. — The prognosis for cure is unfavorable, but the 
patient may live for many } r ears. 

Treatment. — Treatment should be directed to the cerebral 
arterio-sclerosis in order to check the progress of the lesion, 
and in the meantime symptomatic prescriptions of such rem- 
edies as agaricin, mercurius, plumbum, phosphorus, and ta- 
rentula are advisable. In severe cases the tremor may some- 



462 DISEASES OF THE NERVOUS SYSTEM. 

times be controlled by the administration of hyoscin hydro- 
bromate 2x or hyoscy amine 2x, in one grain doses three times 
a day. 

OCCUPATION NEUROSES. 

(Fatigue Neuroses; Writer's Cramp, etc.). 

Etiology. — An occupation which requires the constant repeti- 
tion of certain precise muscular movements may eventually 
lead to fatigue of the sub-cortical motor centre, and this results 
in disturbance of the muscular control necessary for that par- 
ticular maneuver. Writers, pianists, telegraphers, seamstress- 
es, and many others are liable to this neurosis. 

Symptoms. — The onset is usually insidious. The worker 
notices that after a time his hand aches or feels numb, or 
cramped, or tremulous. After a moment's rest he resumes his 
work, but the trouble recurs ; and less and less work becomes 
necessary to induce the disablement, until finally the condition 
is permanent and he is completely incapacitated. The power 
for all other movements remains unimpaired. If no attempt is 
made to resume the occupation the cramp ultimately disap- 
pears; but usually it returns upon any endeavor to take up con- 
tinuously his former work. 

Diagnosis. — The history, and the provocation of the symp- 
toms only by attempts at resuming the occupation, render 
the diagnosis clear. 

Prognosis. — If the patient can completely abstain from his 
customary occupation, the spasm tends to subside and disap- 
pear. He cannot hope to ever again be able to resume his 
former method of work, however. 

Treatment. — The affected muscles must be put at rest, and 
various exercises, massage, electricity, and baths may be em- 
ployed for their general tonic effect. If his vocation cannot be 
changed, the sufferer should learn to use the opposite hand, or 
else some specially constructed apparatus by which the strain 
is taken from the affected motor area. Among the more useful 
remedies are arnica, gelscmium, phosphorus, rhus tox., and 
strychnine. 



DISEASES OF THE NERVOUS SYSTEM. 463 

MIGRAINE. 

(Hemicrania; Sick Headache.) 

Etiology. — This paroxysmal psychoneurosis is obscure in 
nature, though probably cortical in origin. A neuropathic 
heredity and the gouty diathesis seem to act as predisposing 
causes, and it usually makes its appearance in early life, be- 
tween the ages of five and ten years. The exciting cause is 
often difficult to determine; sometimes it is eye strain, and in 
other cases depressed nutrition, indigestion, constipation, 
fatigue, emotional disturbances, lithemia, etc. 

Symptoms. — The only symptoms of migraine are those of the 
attack itself. While these vary somewhat, the following 
stages usually present themselves: 

1. Premonitory symptoms. The patient may for some hours 
be dull and irritable, or suffer with a slight headache. 

2. Sensory symptoms. Suddenly bright spots, colored rings, 
and zigzags or clouds appear before the eyes, or the attack 
may be ushered in by simple dimness of vision. Exceptionally 
taste or hearing is affected, or numbness and tingling are felt 
elsewhere in the body. Rarely motor symptoms, such as 
paresis or motor aphasia, occur at this stage. 

3. HeadacJie. In the course of ten or twenty minutes the 
headache begins. It is usually intense and at first localized to 
one spot, whence it spreads over the rest of the same side or 
involves both sides of the head. It is accompanied by marked 
hyperesthesia of all the senses, and may last for one or many 
hours. 

4. Nausea and vomiting. As the headache reaches its 
height, nausea generally develops and in many cases is fol- 
lowed by vomiting. The latter may be severe and protracted, 
but as it subsides the headache is apt to lessen and the final 
stage, that of 

5. Sleep, supervenes. After a few moments or perhaps 
several hours of slumber the patient awakens free from pain. 



464 DISEASES OF THE NERVOUS SYSTEM. 

Vasomotor symptoms, such as flushing, pallor, and per- 
spiration, sometimes accompany the paroxysm. 

Diagnosis. — The periodical character of the attacks, the 
sensory symptoms with which they are introduced, and the 
nausea and vomiting, serve to distinguish the disease. Even 
in cases less typical the occurrence of these sensory symptoms 
is sufficient to identify the disease. Occasionally it may be 
necessary to exclude organic brain lesions, uremia, or malaria; 
but this is rarely difficult. 

Prognosis. — The prognosis is generally unfavorable. If the 
disease is of recent onset, and the cause can be discovered and 
removed, recovery may ensue. Otherwise it is apt to persist 
in women until the menopause, and until a corresponding age 
in men, when it disappears spontaneously. 

Treatment. — Search for, and if possible remove, the cause. 
Correct eye-strain, improper diet or habits, and all other prob- 
able sources of irritation. The more important internal rem- 
edies, the administration of which should be continued in the 
interval between attacks, are belladonna, calcarea, cannabis 
indica, gelsemium, ignatia, iris, mix vomica, sanguinaria, 
sepia, stanmun, and sulphur. One drop of glonoin 2x taken 
on the tongue will sometimes abort an attack, and in others 
cajfein gr.j-v, has a similar effect. During the paroxysm the 
patient should remain at rest in a darkened, quiet room. 

TRAUMATIC NEUROSES. 

Varieties. — Three classes of conditions may be due to trau- 
matism, viz. : 

1. Injuries of a surgical character. 

2. Traumatic hysteria. 

3. Traumatic neurasthenia. 

Various combinations of these three varieties may also 
present themselves. 

Diagnosis. — Since these conditions are frequently the subject 
of litigation, it is essential that malingering be carefully ex- 



DISEASES OF THE NERVOUS SYSTEM. 465 

eluded. For this purpose it is necessary, if no evidence of an 
actual surgical lesion is present, to apply to the patient the 
same diagnostic methods that would be used for the investiga- 
tion of cases of hysteria and neurasthenia due to other causes. 
The prognosis, when complicated by the question of obtaining 
damages for the injuries received, is less favorable than in 
simple cases; so that prompt settlement of the dispute is de- 
sirable from a physician's standpoint. The treatment is that 
of hysteria and neurasthenia whatever their causes. 

TICS. 

(Mimic Spasm). 

Etiology. — A tic is a spasm identical with a volitional move- 
ment, and probably of subconscious origin. It is apt to appear 
in youth, but no age is exempt; and it frequently represents 
the habit induced by some local irritation (e. g., sniffing due 
to a nasal catarrh, blepharospasm induced by ocular irrita- 
tion). Protracted emotions may induce similar tendencies to 
involuntary facial contortion. 

Symptoms. — These vary according to the location of tic; the 
more important of the latter are as follows: 

Facial tic. This consists of an involuntary lightning-like 
spasm of a muscle or set of muscles, such as blinking the eye 
(blepharospasm), twitching of the nose, grunting, or even 
uttering articulate words {coprolalia). The facial expression 
of ]°Yi grief, fright, or pain ma} T thus be produced, often as an 
indication of some subconscious idea. This spasm may in- 
volve the neck and upper extremities, occasioning various 
attitudes and gestures. 

Spasmodic torticollis (wry neck). This is a spasm of the 
muscles innervated hx the spinal accessory and sometimes 
those supplied by the upper cervical nerve, as a result of 
which the neck is drawn to one side. It is distinct from wry 
neck due to injury or atrophy of the sterno-mastoid before 
birth (congenital torticollis), from wry neck due to rheumatic 
myositis, adenitis, abscess, etc. (symptomatic torticollis), and 
30 



466 DISEASES OF THE NERVOUS SYSTEM. 

from spasm of the neck muscles due to spinal caries {spurious 
torticollis). Mental torticollis is marked by a customary de- 
viation of the head which is spasmodically maintained, but 
which disappears when the patient lies down, or it can be con- 
trolled by slight manual pressure. 

Jumpers and subjects of latali and myriachit impulsively 
obey certain suggestions, often violently and apparently 
against their will, e. g., striking or jumping. 

Treatment. — Correct any possible cause for peripheral irrita- 
tion. Pressure upon certain points in the distribution of the 
fifth nerve inhibits a facial tic; search for such points, and 
having found them, repeatedly check the tic in order that 
ultimately the habit may be arrested. Faradism may have a 
good effect, and even nerve stretching may be employed. 
The patient's self-control should be built up and reinforced by 
suggestion. 

TROPHONEUROSES. 
ACROMEGALY. 

Etiology. — The cause of this disease is practically unknown. 
It usually develops between the ages of eighteen and thirty, and 
is frequently associated with disease of the pituitary body. 

Pathology. — The bones of the face, cranium, and extremities,, 
and to a certain extent those of the trunk, become hyper- 
trophied. The skin and mucous membranes are thickened 
with connective tissue, the kidneys, spleen, and lymphatic 
glands may be sclerosed, the thyroid is often atrophied, and 
the thymus may be persistent and even increased in size. The 
pituitary gland is enlarged and hypertrophic. 

Symptoms. — The head is greatly enlarged and the face is 
strikingly deformed, the thickened skin with deepened fur- 
rows, the thick lips, and the coarse hair giving the features a 
heavy, dull expression. The hands and feet are markedly en- 
larged, especially in width. The complexion is usually sallow, 
and the skin is doughy and does not pit on pressure. The 



DISEASES OF THE NERVOUS SYSTEM. 467 

patient is apt to suffer with intense persistent headache; 
vision is affected, speech may be thick, and sexual power is 
lost. As a rule he is physically weak and mentally sluggish. 
Polyuria, glycosuria, and dyspepsia are common. The reflexes 
are normal or diminished and the electrical reactions may be 
quantitatively reduced. 

Diagnosis. — The disease is slow in its development, extend- 
ing over a period of years, and in its earlier stages may be 
difficult of detection; but when the physical changes are 
marked an error is improbable. Myxedema exhibits a thick- 
ened skin but no bony deformities. 

Prognosis. — The disease, after a duration of twenty or thirty 
years, terminates in muscular weakness and cachexia, and sud- 
den death from heart failure is frequent. 

Treatment is of no avail. At best it can only relieve symp- 
toms, such as headache, by means of appropriate medicines. 



RAYNAUD'S DISEASE. 

(Symmetrical Gangrene). 

Etiology. — The causes of this vasomotor disorder are very 
obscure ; inmany cases anemic and neurotic states appear to 
predispose. The attack may be excited by exposure, severe 
emotional disturbance, or acute infectious diseases. 

Symptoms. — The most striking symptom is the pale, blood- 
less, waxy condition {local syncope) of the fingers and toes, less 
often the ears, nose, or lips. A needle-prick draws no blood, 
and the fingers appear dead (digiti morttii). There is usually a 
sensation of numbness and tingling, with loss of sensibility. In 
a few minutes or hours this may pass off, but in many cases a 
second stage develops, the affected part becoming cyanotic 
and blue-black or red {local asphyxia). In a few hours small 
blebs may appear, and are often followed by ulceration or by 
a dry gangrene which destroys the terminal phalanges or even 
entire fingers. This stage is accompanied by neuralgic pain. 

Constitutional symptoms, such as intermittent hemoglo- 



468 DISEASES OF THE NERVOUS SYSTEM. 

binuria, colic, or uremic convulsions or coma, are frequently 
present. 

Diagnosis. — Care should be taken to exclude gangrene due to 
other causes, including senile gangrene, frost-bite, ergot-poison- 
ing, and obliterating endarteritis. 

Treatment. — Treatment must be directed toward improvement 
of the general health. During the attack, heat or electricity 
may be used locally, and glonoin given internally to relieve the 
arterial spasm. Arsenic or secale may also be indicated. 

ANGIONEUROTIC EDEMA. 

Angioneurotic edema (acute circumscribed edema, giant 
urticaria) is a disease of unknown causation characterized by 
the sudden appearance upon the face, arms, or hands of a cir- 
cumscribed swelling, pale or red in color, and pitting only 
slightly on pressure. There is no actual pain, but itching, 
burning, or stiffness is noted. The swelling disappears in a 
few hours or days, but may recur frequently. By involving 
the larynx {edema glottidis) it may prove fatal; otherwise, the 
prognosis for life is good, but for cure doubtful. The treatment 
must be directed to the patient's general condition, and espe- 
cially to any disorder of the digestive system. 

SCLERODERMA. 

Scleroderma is a rare disease characterized by marked in- 
duration of the skin. The condition is due to the proliferation 
of connective tissue in patches, or in widely diffused areas. 
The thickness of the skin, together with a certain degree of 
muscular atrophy induced by the pressure, results in stiffness 
and impaired mobility. The course of the disease is very 
chronic. The treatment consists of massage, oil inunctions, 
galvanism, warm clothing, and the administration of anti- 
monium cried., bryonia, guaiacuni, graphites, hydrocotyle, lache- 
sis, phosphorus, silica, or stillingia. 



DISEASES OF THE NERVOUS SYSTEM. 469 



FACIAL HEMIATROPHY. 

Facial hemiatrophy is a rare disease characterized by gradual 
atrophy of one-half of the face, the wasting stopping short at 
the median line. The muscles are not paralyzed and the elec- 
trical responses are unaltered. The disease must be distin- 
guished from atrophic palsies due to lesions of the fifth nerve, 
in which paralysis and the reaction of degeneration are present. 
The cause of the disease is unknown. It progresses slowly over 
a long period of time, but finally becomes stationary and does 
not endanger life. Treatment is unavailing. 

INFANTILE CONVULSIONS. 

(Infantile Eclampsia. ) 

Etiology. — Owing to lack of development of the higher cere- 
bral centres in children, the inhibition exercised by them upon 
the lower centres (in the pons Varolii) is weak, and the latter 
react to comparatively slight irritations. In consequence, con- 
vulsions are common in early childhood, especially during the 
first and second years of life, but rapidly decrease in frequency 
as age advances. A neuropathic heredity strongly predisposes 
its victims to convulsive seizures in infancy. 

An infantile convulsion is only a symptom. It may be due 
to: 

1. Gastro-intestinal irritation. This may be the result of 
dietetic errors, indigestion, gastro-enteritis, or the presence of 
worms. 

2. Peripheral irritation. Teething, otitis, phimosis, a 
slight burn, or a mere prick of the skin may cause a convul- 
sion. A foreign body in the respiratory passages, digestive 
tract, or ear may have the same effect. 

3. Acute febrile diseases. The onset of an acute infection, 
notably pneumonia or the exanthemata, may be accompanied 
in children by convulsions. 

4. Disease of the brain or its membranes. Circulatory dis- 



470 DISEASES OF THE NERVOUS SYSTEM. 

disturbances, such as the mechanical congestion following vio- 
lent coughing, meningitis, and gross lesions of the brain, espe- 
cially those inducing the infantile cerebral palsies, may be the 
cause of convulsions. 

5. Rickets is frequently accompanied by recurrent convul- 
sive seizures. 

6. Epilepsy is not seldom the cause of infantile convulsions. 
Symptoms. — As a rule the onset is abrupt, the child becoming 

pale and rigid. Its eyes are fixed, and the eye-balls are rolled 
upward so that only the whites are visible, or there may be 
strabismus. The fingers and toes are inverted, and the face 
becomes cyanotic as the result of impaired respiratory move- 
ment. The child loses consciousness, and it may have involun- 
tary evacuations. The spasm is usually tonic, but it may become 
clonic, as in epilepsy, or it may be so from the beginning. 
Generally at the end of two or three minutes the muscles re- 
lax, and the child falls into slumber. 

Diagnosis. — The symptoms are unmistakable, but the ques- 
tion of etiology is sometimes difficult of solution. Convulsions 
due to indigestion may be limited to a single attack or series of 
attacks. If there be much fever, the onset of an acute infec- 
tious disease may be suspected. If the convulsions are due to 
a brain lesion, they are apt to be repeated and to alternate 
with paralysis. Attacks occurring irregularly and without defi- 
nite cause in children over two years of age are probably 
epileptic. 

Prognosis. — As a rule, in cases due to simple irritation the 
prognosis is favorable. In weakly patients, however, death 
may be brought about by exhaustion. In convulsions sympto- 
matic of other diseases the prognosis is governed largely by the 
character of latter. 

Treatment. — At the moment of the attack loosen the cloth- 
ing, empty the bowel by means of an enema of soap and 
water or oil, and immerse the child in a warm bath (95°). If 
the attack is long-continued, apply cold to the head. Search 
for the cause and remove it if possible. The convulsion itself 
may present indications for the administration of belladonna, 



DISEASES OF THE NERVOUS SYSTEM. T71 

cuprum, cicuta, ignatia, or magnesia p/ios. If it is but a symp- 
tom of another disease, however, the treatment should be 
directed to the latter. 

DISORDERS OF SLEEP. 

Insomnia is a condition of sleeplessness which may accompany 
almost any deviation from health. In certain cases it becomes 
a fixed habit, and may be the only complaint of the patient. 
•Ultimately the lack of proper rest leads to loss of energy, 
courage, good nature, appetite, and digestion; and as a result 
the patient becomes haggard and emaciated. Treatment must 
first be directed to the removal of the causative condition 
(drugs, narcotics, lithemia, uremia, infectious diseases, neuras- 
thenia, intense mental activity, painful affections, etc.), if it 
can be discovered. Improper methods of living should be 
corrected, and appropriate food should be eaten. Sleep may 
be favored by warm baths, not followed by stimulating friction, 
at bed-time. Occasionally a cold pack or an alcohol rub acts 
well. A glass of hot milk, malted milk, or beer at bed-time is 
usually advisable. The administration of belladonna, canna- 
bis indica, toffea, hyoscy amies, opium, Pulsatilla, or stramon- 
ium, when symptomatically indicated, is usually all the medi- 
cation advisable. Remedies powerful enough to induce sleep 
are necessarily dangerous and must not be used with impunity. 
In exceptional cases, however, the physician is justified in 
prescribing chloral hydrate, gr. x-xv, and if there is much 
nervousness, an equal quantity of sodium bromide, in a single 
dose at bed-time. SulpJwnal, gr. x-xx dissolved in a glassful 
of hot water, or a similar quantity of trional, may be preferred 
in some cases. 

Somnambulism is a condition in which the individual, in enact- 
ing his part in a dream, arises and moves about while asleep. 
He retains no waking knowledge of this sleep-walking, but the 
memory of it may be revived during subsequent attacks. The 
condition usually appears in persons of neurotic habit, and 
treatment should be directed to the patient's general state 
rather than to the single symptom. 



472 SUNSTROKE. 

Dreams are perfectly physiological up to a certain point, but 
in connection with lowered physical or mental states they 
may tend to become depressing, terrifying, and distinctly 
pathological. In children pavor nocturnus (night-terrors) is 
not uncommon. The little one awakes from sleep screaming 
with terror and clings to its mother, and some moments 
elapse before it recognizes its surroundings and can be re- 
assured. A similar, though milder, attack is the nightmare 
(incubus) of adults, in which a vivid, terrifying dream disturbs 
the sleep. In many cases these attacks can be traced to indi- 
gestion, imperfect ventilation, worry, fright, etc. Pavor noc- 
turnus is, however, an indication of serious neurotic instability, 
and in a few cases it appears to be an early manifestation of 
epilepsy. Treatment in these cases should, in general, be di- 
rected to the discovery and removal of causative factors. The 
meals should consist of proper food at appropriate intervals,, 
the condition of the alimentary tract should receive attention* 
and indications will be found for the administration of such 
medicines as aconite, belladorma, ciua, Jiyoscyamus, nux vomica, 
Pulsatilla, spigelia, stramonium, sulpJiur, and zinc. 

Narcolepsy, a condition in which the patient repeatedly falls 
asleep during the day, may be a manifestation of hysteria, or 
it may be due to drugs, obesity, uremia, diabetes, syphilis, or 
organic brain disease. Treatment must be directed to the cause. 

Catalepsy, ecstacy, and trance simply represent a prolongation 
of certain stages of the hysterical convulsion. 



SUNSTROKE. 

As the result of exposure to excessive heat two conditions 
may occur, viz. : 

HEAT EXHAUSTION. 

(Heat Prostration.) 
Symptoms. — Heat exhaustion may result from exposure to in- 
tense heat in confined places, such as boiler-rooms or kitchens, 
as well as to the direct rays of the sun. The patient becomes 



SUNSTROKE. 473 

faint, dizzy, nauseated, and sometimes blinded ; the skin is 
pale, cold, and covered with clammy perspiration, the pulse is 
rapid and feeble, and the temperature is subnormal. The 
patient may quickly become delirious or comatose, and actual 
collapse may ensue. The symptoms are supposed to be due 
to vasomotor paresis, as a result of which the blood collects in 
the great abdominal vessels and leaves the brain and the body- 
surface bloodless. In the absence of medical intervention, a 
fatal result is to be apprehended, but under appropriate treat- 
ment recovery is the rule. 

Diagnosis. — Heat exhaustion is distinguished from the oppo- 
site condition of thermic fever by the lowered temperature and 
feeble pulse. Syncope from heart failure or concealed hemor- 
rhage may present identical symptoms, but fortunately the 
treatment is the same in either case. 

Treatment. — If the patient is unconscious, the use of the cold 
tub-bath, as directed for thermic fever, is not contradicted ; in 
fact, the sharp shock, by restoring tone to the vasomotor 
system, is of marked and immediate benefit. Following this, 
and at the beginning in less severe cases, the patient should be 
placed at rest under a blanket, external heat and friction may 
be applied, and occasionally moderate stimulation by means 
of brandy, whiskey, or aromatic spirit of ammonia may be 
required. 

THERMIC FEVER. 

(Sunstroke ; Insolation ; Heatstroke ; Coup de Soleil. ) 

Etiology. — Exposure to intense heat, either that of the sun or 
from furnaces, etc., within doors, is apt to induce high fever, 
particularly when the atmospheric humidity is so great as to 
prevent evaporation from the body surface. Alcoholism strongly 
predisposes to the attack. 

Pathology. — Thermic fever is supposed to be due to interfer- 
ence with the heat centre in the medulla, as a result of which 
more than the normal amount of heat is produced within the 
body and less is thrown off. 



474 SUNSTROKE. 

Symptoms. — There may be a few premonitory signs, such as 
cessation of sweating, dizziness, a sense of oppression, and 
flashes of color before the eyes. Often the victim falls sud- 
denly and is picked up unconscious. His face is flushed, his 
skin hot and dry, the pulse is full and bounding, the breathing 
is labored and sometimes stertorous, and the temperature is 
high (102°-112°). Twitching, jactitation, rigidity, or even 
epileptiform convulsions may occur, and in other cases there is 
active delirium. Frequently the sphincters are relaxed. In 
unfavorable cases the stupor deepens into coma, the pulse 
loses its apparent strength, respiration becomes irregular or of 
Cheyne-Stokes type, and in a few hours the patient dies. In 
the more fortunate cases the temperature falls, consciousness 
gradually returns, and the patient recovers in the course of a 
day or two. Often, however, there persists a certain degree 
of mental enfeeblement or of inability to withstand exposure 
to even moderate heat without return of the headache and 
delirium. This is probably due to a diffuse chronic meningitis 
set up by the sunstroke. 

Diagnosis. — Great care is sometimes necessary in order to dis- 
tinguish sunstroke from other conditions, notably uremia and 
cerebral hemorrhage, or to detect the latter when existing. On 
this account it is essential to examine the heart and the urine 
in every case which does not react promptly to the bath. 
A knowledge of the previous health of the patient, gained by in- 
terrogation of his friends, may aid in diagnosis. The presence 
of paralytic symptoms, hemiplegia or spasm, points, of course, 
to cerebral hemorrhage; but that condition may have antedated 
the sunstroke. 

Prognosis. — This depends upon the severity of the attack, and 
the promptness with which appropriate treatment is applied. 
Nearly a third of the cases prove fatal. 

Treatment. — Immediately place the patient in a bath-tub filled 
with cold water, to which ice is freely added, and rub the sur- 
face of the body vigorously with the cold water or the ice. In 
the course of from five to fifteen minutes, or when a thermom- 
eter placed in the rectum indicates the approach of the tern- 



SUNSTROKE. 475 

perature to normal, wrap the patient in a sheet wrung out of 
ice water, and place him at rest in bed. Administer aconite, 
belladonna, glonoin, or other remedies according to the indica- 
tions present. In some cases abdominal pain and diarrhea 
may be present, calling for such medicines as arsenic, cuprum, 
cuprum ars., podophyllum, oxveratrum alb. Uremic and hemi- 
plegic cases should receive the treatment appropriate to those 
conditions. 



DISEASES OF THE MUSCLES, 



MYOSITIS. 



Etiology. — Inflammation of muscular tissue may be : 

1. Primary, probably infective (rare). 

2. Secondary to infective or toxemic states, notably gout and 
rheumatism (so-called "muscular rheumatism"). 

Exposure to cold air, and especially to draughts, is a common 
exciting cause. In many cases the condition appears to be due 
to the presence of some toxic irritant, probably gouty in nature. 

PRIMARY MYOSITIS. 

Acute simple myositis follows exposure to cold or excessive 
iatigue. The patient complains of lassitude and pains more or 
less severe in the affected muscles, and the latter are tender on 
pressure, and motion is impeded. 

Acute infectious myositis may follow the simple variety, but 
more often its onset is sudden, the patient being seized with a 
chill followed by fever (101°-104°) and general febrile symp- 
toms. x\t the same time there is severe pain in the muscles of 
certain regions, and the latter present a wooden hardness and 
are exquisitely tender on palpation. The overlying skin is dis- 
colored and puffy, and as the result of suppuration of the 
muscles fluctuation may be detected. A vesicular eruption is 
sometimes observed. Pyemic symptoms, fever and sweats, are 
present, and ultimately a typhoid state develops and the 
patient may die of exhaustion between the fifth and sixteenth 
days. In more favorable cases the pains abate, the tempera- 
ture falls, and convalescence becomes established ; but the 
muscular pains and weakness may persist for months. 

Acute infectious poliomyositis. After a prodromal period ex- 
tending over several weeks, during which the patient complains 



478 DISEASES OF THE MUSCLES. 

of lassitude and fatigue, slight edema may be noticed about the 
ankles or face, and small red macules appear on the face, ex- 
tremities, or abdomen. At the same time pain develops in the 
muscles and increases in severity until ultimately the patient 
fears the slightest movement and so lies stiff and motionless in 
his bed. The muscles appear to be contracted, holding the 
limbs in semi-flexion, they do not react to electrical stimula- 
tion, and the deep reflexes are abolished. The patient may 
have a succession of chills, the temperature rises to 104° or 
more, perspiration is abundant, and a typhoid state supervenes. 
Involvement of the respiratory muscles may lead to death from 
suffocation or pneumonia, or it may result simply from exhaus- 
tion. Rarely, the disease recedes and recovery follows a pro- 
longed period of convalescence. 

Chronic or progressive ossifying myositis. In this rare disease the 
muscles undergo progressive calcification. The process gen- 
erally begins in the back of the neck, and consists of the deposit 
of bony plates, or even ossification of entire muscles, through- 
out the body. 

Treatment. — In simple acute myositis rest and the administra- 
tion of such remedies as arnica, cimicifnga, gelsernium, Pulsa- 
tilla, or rJius tox. usually brings about recovery. Should the 
myositis merge into the suppurative form, the parts may be 
wrapped in a moist, weakly antiseptic, dressing, and as soon as 
pus is detected it must be evacuated and the cavity treated on 
surgical principles. Hepar, mercurius, silica, or sulphur may 
be given internally, and the patient's strength must be sus- 
tained by means of highly nutritious food and alcoholic stim- 
ulants. 

In acute infectious poliomyositis and in the ossifying form 
no treatment appears to be of any avail. 

SECONDARY MYOSITIS. 

Etiology. — Muscular tissue may become inflamed through ex- 
tension of the process from adjacent lesions (e. g., arthritis) or 
through the action of toxins, usually bacterial in nature. The 



DISEASES OF THE MUSCLES. -479 

muscular degeneration which accompanies the acute infectious 
fevers, notably typhoid, is often overshadowed by the symp- 
toms of the primary disease. In syphilis and tuberculosis in- 
flammation of the muscles may constitute an important feature 
of the disease. A distinct type is, however, afforded by — 

Rheumatic myositis (muscular rheumatism, myalgia). This is 
probably more often due to gouty or other diathetic states than 
to rheumatism. It is characterized by severe pain in certain 
muscles, such as the sterno-mastoid (torticollis), the shoulder 
muscles (omalgia), the dorso-lumbar muscles (lumbago), the 
intercostal muscles (pleurodynia), etc. The only invariable 
symptom is pain, but in addition the muscle is sometimes 
swollen, and in some cases there is a slight rise of temperature 
(100°). The condition may be acute, lasting but a few days, 
or it may be chronic and of long duration. The diagnosis rests 
upon the exclusion of neuritis (localized pain and tenderness 
over large nerve trunks) and neuralgia (less affected by motion 
or heat, more paroxysmal, etc.). 

Treatment. — Place the muscles at rest. Apply dry heat by 
means of a hot water bag or a warm flat-iron. Massage the 
muscle daily, and administer such remedies as arnica, cimici- 
fnga, mezereum, and rhus tox. Chronic cases may require 
persistent massage, passive motion, and electricity. 

MYOTONIA CONGENITA. 

(Thomsen's Disease.) 

This is a rare disease, congenital and hereditary, character- 
ized by a painless tonic spasm of the muscles, lasting but a few 
seconds, which develops whenever voluntary motion is at- 
tempted. After motion has begun it proceeds with facility. 
The muscles themselves are hypertrophied, sensibility and re- 
flexes are normal, and the application of either the galvanic or 
faradic current induces a normal contraction. The latter de- 
velops and relaxes very slowly, however, and during the pass- 
age of the galvanic current vermicular, wave-like contractions 



480 DISEASES OF THE MUSCLES. 

pass from the cathode to the anode (the myotonic reaction of 
Erb). The disease is incurable, but does not tend to shorten 
life. 



PROGRESSIVE MUSCULAR DYSTROPHY. 

Etiology. — In adition to varieties of muscular atrophy due to 
disease of the lower neuron, there are several forms of muscu- 
lar wasting apparently due to primary disease of the muscles 
themselves. In a majority of cases these conditions are hered- 
itary and represent a congenital tendency to defective devel- 
opment. 

Pathology. — The muscular tissues may early show an increase 
of connective tissue and perhaps some hypertrophy of the 
muscle fibres, but the latter is ultimately followed by degener- 
ation and atrophy of the fibres, together with a deposit of fat 
about them. 

Symptoms. — The features distinguishing progressive muscular 
dystrophy from progressive muscular atrophy of spinal origin 
are : 

1. Development in early life. 

2. The occurrence of true or false hypertrophy of the muscles. 

3. The absence of fibrillary twitchings. 

4. The absence of the reaction of degeneration. 

Varieties. — 1. Pseudo-hypertropliic paralysis. This form is 
characterized by — 

(a) Weakness in certain muscles, especially those of the 
calves, and a waddling gait. 

(/?) A peculiar difficulty in rising from the ground, to over- 
come which the patient places his hands on his knees and 
"climbs up himself." 

(<r) An apparent increase in the size of the muscles, particu- 
larly those of the leg and sometimes of the shoulder. 

The condition is due to increase of the connective tissue and 
fat, associated with atrophy of the muscle fibres. Later, how- 



DISEASES OF THE MUSCLES. 481 

ever, the entire mass becomes wasted, and contractions in the 
affected muscles lead to deformities (talipes equinus, etc). 

2. The " juvenile form" of Erb is characterized by — 

(a) Progressive atrophy and weakness of many muscle 
groups, especially those of the shoulder, upper arm, gluteal 
region, and thigh. The forearm and leg muscles are involved 
late in the course of the disease or not at all. 

(b) The disease usually begins in the adolescent period, be- 
tween the loth and 20th years, and is apt to affect several 
members of the same family. 

3. The "infantile form" or Landouzy-Dejerine type dif- 
fers from that last mentioned only in the involvement of the 
face muscles. It gives the patient a peculiar, dull expression — 
the "myopathic facies," in which the lips are separated, the 
lower one being unduly prominent, and the patient is unable to 
pout. The other muscle-groups are affected as in the Erb 
type. 

Diagnosis. — The diagnosis rests upon the discovery of obvious 
muscular weakness and wasting unassociated with the reaction 
of degeneration or other evidences of disease of the lower 
neuron. 

Prognosis. — The course extends over years, but ultimately in- 
volvement of the respiratory apparatus or of the heart, or else 
an intercurrent disease, leads to a fatal termination. 

Treatment. — Carefully selected and graduated exercises for the 
weakened muscles, together with massage, electricity, and 
general nutritional measures, should be tried. In the pseudo- 
hypertrophic variety, aurum, kali iod., or phosphorus maybe 
prescribed. In other cases argent, nit., arnica, arsenic, baryta, 
■cuprum, gelsemium, mercurius, physostigma, plumbum, and 
sulphur may be considered. 



31 



THE INTOXICATIONS. 



ALCOHOLISM. 



Symptoms. — The intemperate use of alcohol may manifest 
its effects in three ways, viz. : 

1. Acute alcoholism (inebriety, drunkenness). The amount 
of alcohol required to induce this condition varies greatly, and 
the manifestations likewise differ in different individuals. As 
a rule, however, the primary effect is one of excitement, with 
bright eyes, flushed face, and ungoverned tongue. Then the 
well-known staggering gait develops, speech gradually becomes 
incoherent, and the drunken man finally falls into a deep sleep, 
from which he can be partly aroused only to sink back into 
his stupor. 

2. Chronic alcoholism. Persistent intemperance in the use of 
alcohol ultimately leads to chronic gastritis, hepatic cirrhosis, 
arterio-sclerosis, and other degenerative changes in the tissues. 
In the meantime it produces man) 7 more or less characteristic 
symptoms, notably muscular unsteadiness, indicated by tremor 
of the legs, hands, and tongue, and mental sluggishness with 
impaired will power, defective judgment and poor memory. 
Gastric catarrh is evident in the loss of appetite, coated tongue, 
foul breath, constipation, and morning nausea. Dilatation of 
the stomach and fatty infiltration of the liver are particularly 
common in beer-drinkers. Multiple neuritis, meningitis, and 
insanity are less common sequelae. 

3. Delirium tremens {mania a potii). As the result of the 
long continued action of alcohol on the brain, and often ap- 
parently as a direct sequence to withdrawal of the customary 
stimulation, this peculiar variety of delirium develops. At first 
the patient is sleepless and intensely restless, and then he be- 
gins to have visual hallucinations, believing himself pursued 



484 THE INTOXICATIONS. 

by serpents, rats, and various horrible monsters. His terror 
is pitiable. Frequently he becomes unmanageable in his efforts 
to escape his visionary foes, and even suicide is not uncommon. 
Auditory hallucinations may also be present. The muscles are 
tremulous, the tongue heavily coated, there is moderate fever 
(102°-103°), and a weak pulse. The patient may continue in 
this condition for the greater part of a week, recovery being 
heralded by his falling asleep. In other cases a fatal termina- 
tion is brought about by vital failure. 

Treatment. — Acute alcoholism requires little direct treatment; 
as a rule it is enough to allow the patient to sleep off his in- 
toxication and then prescribe capsicum, mix vomica or other 
indicated remedy. Occasionally it is desirable to empty the 
stomach, and for this purpose tickling the fauces or compell- 
ing the patient to swallow an emetic of mustard and warm 
water (a heaping teaspoonful to the pint) is effective. 

In chronic alcoJiolism, unless delirium tremens is present, it 
is wise to completely withdraw the intoxicant at once. If 
necessary, trional, gr. xv, or hyoscin hydrobromate, gr. y-g-o, 
may be administered to induce sleep. An abundance of highly 
nutritious food should be given, tea and coffee may be taken 
freely, and such medicines 2J$>arsenicum, mix vomica, strychnine, 
or sulphur may be prescribed. Unfortunately, attempts at ref- 
ormation are rarely successful. Only by means of a certain 
degree of restraint, such as an institution alone affords, can 
abstinence be secured, and even in cases thus controlled re- 
lapse is the rule. 

Delirum tremens necessitates control of the patient by attend- 
ants and at times by physical means, such as a folded sheet 
or straps. Forced feeding is advisable, the patient being 
given, at frequent intervals, small quantities of milk, eggs, and 
soup. Such remedies as belladonna, hyoscyamus, and stramo- 
nium are sometimes sufficient to master the delirum, but in 
many cases the attendant is justified in giving hyoscin hydro- 
br ornate, gr. -§-§, or, if there is no nephritis, morphia., gr. % , 
hypodermatically, in order to induce sleep. The depression 



THE INTOXICATIONS. 485 

following- the withdrawal of alcohol may be combatted by 
the administration of aromatic spirit of ammonia or strychnine. 

MORPHINISM. 

Symptoms. — The morphine habit usually follows long con- 
tinued use of that drug, under a physician's orders or otherwise, 
for the relief of some painful affection. The constant craving 
for morphine requires increasingly larger doses for its satisfac- 
tion, and often the patient goes on periodical morphine sprees. 
In the meantime a characteristic change comes over the victim's 
mentality. He is irresolute, lacks self-control, and is untruth- 
ful to a degree. As the time for another dose approaches, he 
becomes restless, mentally depressed, and intensely anxious, 
with a sense of impending evil. These symptoms are tempo- 
rarily relieved by the drug, but return and are greatly intensi- 
fied should the morphia be withdrawn entirely. If the habit is 
continued, the patient develops neuralgic pains, tremor, paresis, 
and rarely ataxia. Should he reach an advanced age, he 
becomes sallow and wizened ; but as a rule long before that 
period he has fallen an easy victim to some intercurrent dis- 
ease-. 

Treatment. — It is almost absolutely necessary that the patient 
be placed in an institution under charge of a separate nurse, 
for in this way alone can the supply of the drug be cut off. 
Morphine should be completely withdrawn at once, the result- 
ing vomiting, diarrhoea, and insomnia being treated symptom- 
atically. The patient should be nourished with milk and 
cream, beef juice, or broths ; and aromatic spirit of ammonia 
or strychnine may be administered to combat the depression. 

CHLORALISM. 

The habitual use of chloral leads to mental deterioration and 
weakness, and even to a mild melancholia. Various skin erup- 
tions may develop, or, in their absence, slight exertion or 
alcoholic stimulation may suffice to produce an intense erythe- 



486 THE INTOXICATIONS. 

matous redness of the skin. This is probably the result of 
vasomotor instability. The treatment is similar to that of 
morphinism. 

COCAINISM. 

The habitual use of cocain leads to rapid moral deterioration, 
with volubility of speech, bright eyes and dilated pupils, hal- 
lucinations of sight, smell, and hearing, and morbid suspicions 
or delusions of persecution. Mild convulsive seizures and 
nystagmus are sometimes noted. The treatment, fortunately 
more efficacious than in the case of morphinism, consists in the 
withdrawal of the drug, and the administration of nourishing 
food, and non-intoxicating stimulants. 



PLUMBISM. 

(Lead-Poisoning; Saturnism.) 

Etiology.— Lead may enter the system by the respiratory pas- 
sages, the digestive tract, or the skin. It affects principally 
workers in lead, painters, plumbers, and glaziers. Occasion- 
ally poisoning results from the use of hair-dyes, cosmetics, or 
canned foods. 

Symptoms. — The manifestations of lead-poisoning are some- 
times rapid in their development, while in other cases they ex- 
tend over a long period of time. Colic is a striking symptom; 
it consists of severe pain, often paroxysmal, in the region of the 
umbilicus; the abdomen is not distended, as in cases of flatu- 
lent colic, but flat, and the pulse may be markedly slowed. 
Muscular cramps, especially affecting the flexor muscles of the 
arms and legs, and pains in the region of the joints {arthralgia 
saturnind) are common. Constipation, a blue line on the gums 
at the point of contact with the teeth, and anemia attended by 
a sallow skin {icterus saturninus) are usually present. 

Muscular paralysis, especially affecting the extensors, and 
leading in typical cases to wrist-drop, is a serious result of 
lead-poisoning. The paralysis may affect single muscles or 



THE INTOXICATIONS 487 

groups of muscles, it is usually bilateral, is often accompanied 
by tremor, and may eventuate in rapid muscular atrophy, as- 
sociated with the reaction of degeneration. Involvement of 
the central nervous system {lead encephalopathy) may pro- 
duce such conditions as amaurosis, optic neuritis, headache, 
stupor, delirium, mania, convulsions, or insanity. Gout and in- 
terstitial nephritis are also well-known consequences of lead- 
poisoning. 

Diagnosis. — The diagnosis rests upon the history of exposure 
to lead, the blue line on the gums, and the presence of some 
of the symptoms detailed above. 

Prognosis. — This depends upon the degree to which the system 
is saturated with lead, and the extent of the changes induced 
by that poison. Colic and constipation are usually relieved 
by treatment, arthralgia and palsy are less hopeful, the pre- 
sence of muscular atrophy constitutes an unfavorable symptom, 
and encephalopathy and chronic nephritis are rarely cured. 

Treatment. — The intense pain of lead colic may be relieved by 
hot applications or a hot bath, and the use of such remedies as 
alumina, belladonna, mix vomica, and platina. Rarely an 
opiate is necessary. Constipation may be relieved by the use 
of opium. 

The elimination of lead from the system is favored by the 
persistent use of hot baths, attention to the activity of the 
bowels, and the use of sodium iodide, gr. j-v, taken in half a 
glassful or more of water before meals. Faradism may be ap- 
plied to paralysed muscles, and nourishing food aids in com- 
bating the anemia. The patient must, of course, change his 
occupation if permanent recovery is to be secured. 



ARSENICAL POISONING. 

Etiology. — Arsenical poisoning may be acute, following the 
ingestion of Paris Green or " Rough on Rats," or it may be 
chronic, developing in those who occupy apartments decorated 
with arsenical wall-paper, or in those engaged in handling 



488 THE INTOXICATIONS. 

artificial flowers or clothing containing the poison. It may 
follow the long-continued medicinal use of the drug. 

Symptoms. — Acute arsenical poisoning is attended by intense 
abdominal pain, vomiting, and diarrhea, and these symptoms 
may speedily be followed by collapse and death. These chole- 
raic symptoms are frequently associated with albuminuria, 
skin eruptions, and, if life be prolonged, paralysis from arseni- 
cal neuritis. 

Chronic arsenical poisoning is attended by symptoms of 
debility, with anemia, gastro-intestinal irritability, gastralgia, 
and vague nervous symptoms. Multiple neuritis, with its 
characteristic "steppage" gait, may ensue. 

Treatment. — In cases of acute arsenical poisoning, neutralize 
some solution of ferric chloride with sodium carbonate or mag- 
nesia, collect the precipitate on muslin or filter paper, and ad- 
minister it freely to the patient. In cases of extreme emer- 
gency, dialyzed iron, tincture of ferric chloride, or Monsel's 
solution may be given. If the stomach has not already emptied 
itself, administer in addition an emetic of mustard and water,, 
then wash out the stomach by giving copious draughts of warm 
water, and later administer castor oil in order to carry off the 
poison from the bowels. 

Chronic arsenical poisoning requires discovery and removal 
of its source, together with symptomatic treatment of the 
symptoms as they arise. 

PTOMAINE POISONING. 

(Food- Poisoning ; Bromatotoxismus. ) 

Etiology. — Ptomaines, substances resulting from the bacterial 
decomposition of organic matter, vary in their toxicity. De- 
composed meats, milk, cheese, ice cream, fish, and shell-fish 
are among the more common substances, the ingestion of 
which as food is followed by symptoms of acute poisoning. 

Symptoms. — At the end of a period ranging from one to forty- 
eight hours after the ingestion of the contaminated food, the 



THE INTOXICATIONS. 489 

patient is seized with nausea, vomiting, cramps, and diarrhea. 
In addition there may be constriction of the throat and dif- 
ficulty in swallowing, headache, vertigo, dimness of vision, and 
extreme prostration. Severe cases may closely simulate cholera, 
the patient perishing in collapse. 

In certain cases of poisoning by shell-fish, however, the 
poison seems to concentrate its attack upon the nervous system. 
There is intense burning and itching of the face and sometimes 
the entire body, followed by the appearance of a vesiculo- 
papular eruption ; and the patient becomes dyspneic, the face 
is livid, and delirium, unconsciousness, convulsions, and coma 
may ensue. At other times the symptoms are simply those of 
collapse. Death may occur at any time within a week. 

Treatment. — If there is any question as to whether the vomit- 
ing and purging have cleared the alimentary tract of its con- 
tents, a purge may be administered. Stimulants must be 
given freely, should collapse threaten ; and the symptomatic 
indications are usually present for arsenicum, belladonna> 
bryonia, capsicum, creosote, nux vomica, or pJiosphoric acid. 



ANIMAL PARASITIC DISEASES. 



The parasites which infest the body of man are great in 
numbers and variety, but the majority of them are harmless. 
In some cases, however, they are directly injurious, and upon 
their discovery and removal depends the relief of symptoms 
more or less serious. Of this class of parasites, the various 
worms are by far the most important, and the commoner 
forms of the latter are as follows: 

1. Cestodes (tape-worms). 

2. Trematodes (flukes). 

3. Nematodes (round worms, thread worms). 

CESTODES. 

( Tape-Worms. } 

A tape-worm consists of a head (scolex) and joints {proglot- 
tides^). Reproduction is by sexual alternation. The bisexual 
segments breed from the head and the impregnated eggs enter 
the stomach of some second animal, the intermediate host, 
where the embryo becomes liberated by the digestion of its 
covering, and then migrates to other organs, where it forms an 
encysted larva (cystieereus). Meat containing these cysticerci 
is said to be "measly;" should it be eaten without proper 
cooking by man, the worm develops into maturity in the in- 
testines of the latter. Three varieties are common, viz. : 

1. Taenia solium (pork tape-worm). This parasite is from six 
to eight feet long. The head, of pin-head size, is provided 
with four suckers and a double row of hooklets, and is attached 
to its body by a threadlike neck about an inch long. Each 
body-segment contains male and female generative organs, 
and becomes larger and more mature, the greater its distance 
from the head. 



492 ANIMAL PARASITIC DISEASES. 

2. Taenia saginata or mediocanellata (beef tape-wormj is longer 
than the taenia solium, the sexual organs in each segment are 
somewhat different, and the head possesses four suckers but no 
hooklets. This is the variety most common in the United 
States. 

3. Bothriocephalus latus (fish tape-worm) has a club-shaped 
head provided in the median line with grooves which act as 
suckers. The segments are short and broad; and the parasite 
is frequently from twenty-five to thirty feet in length. 

Symptoms. — The symptoms arising from the presence of a tape- 
worm in the alimentary tract are mainly irritative in character, 
e. g., abdominal pains, nausea, meteorism, and an inordinate 
appetite. In addition, various nervous symptoms, such as 
itching of the nose and anus, vertigo, palpitation, headache, 
choreiform movements, epileptiform convulsions, and marked 
anemia, may develop. The presence of the parasite is often 
unsuspected until a segment is passed with the dejecta. Only 
by the discovery of such a segment or of the ova in the stools 
can a diagnosis be made. 

Rarely the embryos migrate into the tissues of the human 
body and there become encysted (cysticerci cellulose?). In the 
brain or cord their presence sometimes gives rise to the local- 
izing indications of a tumor; owing to their development in 
subcutaneous tissues there may be stiffness on motion; and in 
the skin they may appear as multiple tumors varying in size 
from that of a pea to that of a bean. 

4. Taenia echinococcus, the smallest of the tape-worms, is, when 
fully matured, about one-fourth of an inch in length and pos- 
sesses four segments, the first of which, the head, is provided 
witharostellum, four suckers, and a double row of hooklets. It 
infests the larger breeds of dogs. In man it occurs only in the 
larval state, forming echinococcus cysts. The latter may be 
found in any portion of the body ; the liver is, however, most 
frequently invaded. Hydatid cyst of the live}' occasions 
symptoms which vary according to the size and situation of the 
growth. A sensation of dragging and pain may be felt in the 



ANIMAL PARASITIC DISEASES. 493 

hepatic region. Upward displacement of the diaphragm is 
apt to cause cough and dyspnea ; pressure on the portal vein 
may lead to ascites ; pressure upon the bile ducts sometimes 
occasions jaundice. More significant, however, are the physi- 
cal signs: fulness in the hepatic region, an increased area of 
liver dulness, a fluctuating mass or masses, and the hydatid 
thrill (see page 289). 

Diagnosis may be made positive by discovery of the character- 
istic hooklets in the aspirated or discharged contents of the sac. 
The case may end fatally in the absence of surgical interven- 
tion; following the latter, recovery is usual. 

Treatment. — In order to dislodge any variety of these para- 
sites from the intestine, the patient must for two days be 
allowed only a light diet. On a third day nothing but a little 
gruel or milk should be permitted, and at the same time the 
administration of a saline purge is advisable Then, at bed- 
time, give thirty minims of ethereal extract of male fern , and 
in the morning sixty minims more of the same remedy. A 
few hours later administer a purge, preferably of castor oil ; 
and watch the stools, in order to be certain, if possible, that 
the head of the parasite is passed. 

Among other effective anthelmintics are infusion of pome- 
granate (two ounces of the bark in a pint of water), kooso 
flowers (half an ounce in half a pint of water) and pumpkin 
seeds (one or two ounces of the powdered seeds mixed with 
some pleasant substance ) . The preparatory steps in the treat- 
ment must be the same, whichever remedy is used. 

TREMATODES. 

(Flukes.) 

1. Liver flukes {distoma hepatictim, etc.) are found in the bile 
passages and the upper intestine. When numerous they are 
capable of giving rise to cholangitis, hepatic enlargement, 
diarrhea, and ascites. The ova may be discovered in the 
stools. 



494 ANIMAL PARASITIC DISEASES. 

2. Blood flukes {distoma hematobium) are common only in the 
tropics. They inhabit the venous system, especially the portal 
vein and its tributaries, and give rise to diarrhea, ulcerations of 
the mucous membrane, and hematuria. The ova may be 
recognized in the urine. 

3. Bronchial flukes (distoma pulmonalis) are met with in China, 
Japan and Formosa, where they infest the bronchial tubes and 
cause cough and hemoptysis. 

NEMATODES. 

1. Ascaris lumbricoides (round worm) resembles the ordinary 
earth worm in appearance, being brownish in color and vary- 
ing from six to eighteen inches in length. Large numbers of 
this parasite may be present in the human intestine, and occa- 
sionally they migrate into the bile ducts, the stomach, or rarely 
into the air passages or even the Eustachian tube. As a rule, 
these worms are harmless, but in some cases they induce symp- 
toms of gastro-intestinal irritation, or, in children, itching of 
the nose, grinding of the teeth, disturbed sleep, and even con- 
vulsions. A satisfactory diagnosis is possible only through the 
expulsion of one or more worms, but when the presence of the 
latter is suggested by these vague symptoms the patient should 
receive such remedies as cina, belladonna, cicuta, lycopodium, 
mercurius, mix vomica, podophyllum, sabadilla, spigelia, and 
sulphur. Should these remedies prove insufficient, santonine y 
gr. %-], three times a day, or naphtalin, gr. iij-xx, t. i. d., fol- 
lowed by a mild purge of calomel, may be given. 

2. Oxyuris vermicularis (pin worm ; thread worm) is a small 
worm common in and peculiar to man. The female is about 
half an inch, the male about one-quarter of an inch, in length. 
They are actively mobile. As long as they remain in the ileum 
and large intestine they give rise to no symptoms, but should 
the rectum be invaded, itching of the anus, especially at night, 
becomes very troublesome, and by invasion of the vagina in- 
tense itching and even catarrhal inflammation of that region 
may be produced. If the worms are not expelled from the 



ANIMAL PARASITIC DISEASES. 495 

body after the administrasion of cina, mercurius, teucrium, 
sulphur, or other indicated remedy, give mercurius dulcis lx, 
gr. iii, every two hours until the bowels are moved freely, and 
follow this by the use of a profuse enema of soap and water, or 
of plain water followed by two or three ounces of infusion of 
quassia. Scrupulous cleanliness must be observed, lest by con- 
veyance of the ova to the mouth reinfection should occur. 

3. Trichina spiralis is a small worm derived from the hog. It 
enters the human body with imperfectly-cooked food and is set 
free in the stomach, where it propagates. In the course of a 
week the living embryos thus brought forth work their way 
through the intestinal wall into the blood-current and are car- 
ried to the muscles, where they assume a spiral form and be- 
come encapsulated. Thus they may live for years. During 
their presence in the alimentary tract the symptoms are irrita- 
tive in character — nausea, vomiting, abdominal pain, and diar- 
rhea, which, in severe cases, suggest cholera. In the course 
of a week or two muscular symptoms develop, the muscles be- 
coming swollen, tender, and extremely painful. The skin, espe- 
cially of the eyelids, may be edematous. There is considerable 
fever (100°-104°), sweating is profuse, albuminuria may be 
present, and typhoid fever is suggested by the symptoms. The 
disease is often fatal, about one-third of the cases succumbing 
to pulmonary complications. Diagnosis is usually based upon a 
knowledge of the infection of a number of individuals by the 
same meat. Blood examination frequently reveals marked 
eosinophilia, and insoection under the microscope of a small 
bit of muscle, excised under cocain-anesthesia, may reveal the 
presence of the encysted parasite. 

Prophylaxis may be secured by thorough inspection of all 
meats offered for sale, and proper cooking of that which is in- 
tended for the table. Treatment consists of clearing out the 
bowels by repeated brisk purges, followed by the administra- 
tion of glycerine, 3ss, every hour, or thymol, 5j in caps. When 
the trichinae have invaded the muscles, remedies should be 
prescribed according to the symptomatic indications present. 



496 ANIMAL PARASITIC DISEASES. 

4. Anchylostoma duodenale {strongylus duodena lis) is a short 
cylindrical worm found in the upper portion of the small in- 
testine. It is rare in the United States, but is quite common 
in Egypt, Italy, India, and Brazil. It is of great diagnostic 
importance, because by its constant sucking of blood from the 
intestinal walls it produces an anemia so profound that it may 
be classed as pernicious {Egyptian chlorosis ; St. Got hard's 
disease). Gastro-intestinal symptoms are marked : there may 
be anorexia, nausea, vomiting, abdominal pain, and some- 
times obstinate diarrhea. The diagnosis rests upon discovery of 
the eggs in the stools. The disease tends to a fatal issue in the 
course of weeks or months, but cure can be effected by appro- 
priate treatment. The latter consists of the administration of 
etherial extract of male fern, 3i-ii, or of tJiymol, 3ss every hour 
for four doses, followed by a purge. 

5. Tricocephalus dispar (whip-worm) is found in the large intes- 
tine in man. It is from one-half an inch to two inches in 
length, and is called "whip-worm" because of the resem- 
blance of a long spiral thread attached to its head to the lash of 
a whip. It possesses little diagnostic importance. The treat- 
ment should be that advised for ascaris lumbricoides. 

6. Fiiaria sanguinis hominis is found principally in the tropics. 
The mature worm is about three inches in length. The para- 
site makes its normal habitat in the lymphatic vessels of the 
human body; its embryos swarm in the patient's peripheral 
blood vessels during the hours of rest, but disappear during 
the working hours of the day. The infection of man {filar ia- 
sis) occurs through the agency of the mosquito. Through 
blocking of the lymph-channels by the adult worm or its ova 
cJiyluria may be caused (see page 195). The chylous urine 
may or may not be mixed with blood. The parasites are 
found in abundance in the sediment. Lymphatic stenosis 
may also lead to elephantiasis of the lower extremity. Treat- 
ment is usually unavailing, although methylene blue., gr. ij in 
caps. t. i. d., may be tried, and in the meantime medicines 
should be prescribed according to the symptomatic indica- 
tions present. 



INDEX. 



Abdominal dropsy, 285. 

Abdomen, external examination of, 
241. 

Abdomen, hysterical, 284. 

Abdominal typhus (see Typhoid), 25. 

Abnormal contents of bowel, caus- 
ing obstruction, 271. 

Abdominal reflex, 387. 

Aboulia, 445. 

Abscess of brain, 407. 

of the liver, 293. 
of the lung, 180. 
of spleen, 318. 
perinephritic, 277. 
retropharyngeal, 238. 
subdiaphragmatic, 184, 292. 
subphrenic, 292. 

Absorbent function of stomach, test 
for, 245. 

Accommodation, reaction to, 368. 

Acetonuria, 201. 

Achromatopsia, 444. 

Achylia gastrica, 252. 

Aceto-acetic acid (see Diaceticacid), 
201. 

Acids, combined, in stomach con- 
tents, test for, 244. 

Acid, free hydrochloric, in stomach 
contents, test for, 243. 

Acid, lactic, in stomach contents, 
test for, 244. 

Acids, organic, in stomach contents, 
test for, 244. 

Acromegaly, 466. 

Actinomycosis, 86. 

Acute ascending paralysis, 419. 

Acute articular rheumatism (see 
Rheumatic Fever), 51. 

32 



Acute bulbar paralysis, 410. 
Analgesia, tests for, 386. 
Addison's disease, 343. 
Adherent pericardium, 122. 
Adhesive pylephlebitis, 313. 
Adipositas universalis, 359. 
Adrenal bodies, diseases of, 343. 
Aginesis, 411. 
Agraphia, 364. 

Air, conveyance of infection by, 18. 
Air passages, upper, examination of, 

148. 
Albuminoid liver, 299. 
Albumin, quantitative estimation of, 

199. 
Albumin, tests for, 199. 
Albuminuria, 198. 
Alcoholic neuritis, 437. 
Alcoholism, 483. 
Alexia, 364. 

Algid stage of Asiatic cholera, 60. 
Alimentary glycosuria, 350. 
Amaurosis, 365. 
Amblyopia, 365. 
Amblyopia, hysterical, 366. 
Amimia, 364, 365. 
Amnesia, 445. 
Amnesic aphasia, 364. 
Amoebic dysentery, 43. 
Amphoric breathing, 163. 
Amyloid degeneration of the heart, 

136. 
Amyloid kidney, 218. 
Amyloid liver, 299. 
Amyloid spleen, 319. 
Amyotrophic lateral sclerosis, 425. 
Anarthria, 363. 
Anchylostoma duodenale, 496. 



498 



INDEX. 



Anemia, cerebral, 396. 

chlorotic, 332. 

infantum pseudo-leuke- 
mica, 338. 

lymphatic, 337. 

pernicious, 332. 

post-malarial, 49. 

secondar}-, 330. 

splenic, 336. 

symptomatic, 330. 
Anemic murmurs, 119. 
Anesthesia, examination for, 385. 
Anesthesia, hysterical, 443. 
Aneurism, 142. 
Aneurism of the abdominal aorta, 

144. 
Aneurism of the ascending arch, 144. 
descending arch, 144. 
thoracic aorta, 142. 
transverse arch, 144. 
Angina pectoris, 138, 
Angioneurotic edema, 468. 
Animal parasitic diseases, 491. 
Ankle clonus, 389. 
Ankle jerk, 38S. 
Anopheles, 45. 
Anosmia, 365. 
Anterior poliomj-elitis, acute. 423. 

chronic, 424. 
Anthrax, 82. 

Antitoxin, use of, in diphtheria, 63. 
Aorta, aneurism of, 142. 
dilatation of, 128. 
Aortic area, auscultation of, 117. 
Aortic insufficiency, 127. 
Aortic obstruction (see Aortic Steno- 
sis), 128. 
Aortic regurgitation, 127. 
Aortic stenosis, 128. 
Aortitis, 128. 
Aphasia, 363. 

motor, 364. 
sensory, 363. 
Aphemia, 364. 



Aphthae (see Aphthous Stomatitis), 
232. 

Bednar's, 233. 
Apoplexy, cerebral, 398. 
Appendicitis, 274. 

catarrhal, 275. 
circumscribed, 275. 
endo-, 275. 
interstitial, 275. 
parietal, 275. 
peri-, 275. 
recurring, 276. 
relapsing, 279. 
Aran-Duchenne type of muscular 

atrophy, 424. 
Area, aortic, auscultation of, 117. 
of deep cardiac dulness, 1 [6. 
of superficial cardiac dulness, 

116. 
mitral, 116. 
pulmonic, 117. 
tricuspid, 117. 
Argyll-Robertson pupil, 368, 431. 
Argyria, 344. 
Arhythmia, 137. 
Arsenical neuritis, 436, 488. 

poisoning, 487. 
Arterio-capillary fibrosis, 140. 
Arterio-sclerosis, 140. 
Arthralgia saturnina, 486. 
Arthritis deformans, 356. 

rheumatoid, 356. 
Arthropathies, 431, 434. 
Articular rheumatism (see Rheu- 
matic Fever) ,51. 
Ascaris lumbricoides, 494. 
Ascending nephritis (see Pyelo- 
nephritis}, 219. 
Ascites, 285. 
Asiatic cholera, 59. 
Asphyxia, local, 467. 
Aspiration, in empyema, 187; in peri- 
cardal effusion, 123; in pleuritic 
effusion, 187. 



INDEX. 



499 



Astasia-abasia, 446. 
Asthma, 171. 
Ataxia, 383. 

Friedreich's, 429. 

hereditary, 429. 

hereditary cerebellar, 429. 

locomotor, 430. 

progressive spastic, 427. 

static, 430. 
Ataxic gait, 430. 
Ataxic paraplegia, 427. 
Atelectasis, 181. 
Atheroma, 140. 
Athetosis, 384. 
Atonic dyspepsia, 261. 
Atrophic rhinitis. 151. 
Atrophic pharyngitis, 237. 
Atrophy, acute yellow, of liver, 300. 
Atrophy of the heart, 136. 
Atrophy, progressive muscular, 

spinal, 424. 
Auditor}- aphasia, 363, 364. 
Auditor}^ hyperesthesia, 371. 
Auditory nerve, 370. 
Autumnal catarrh (see Hay Fever), 
152. 

Bacillus of anthrax, 82. 

of cholera, 59, 60. 

of glanders, 84. 

of influenza, 40. 

of leprosy, 109. 

of Pfeiffer, 40. 

of plague, in. 

of tuberculosis, 87, 101. 

Klebs-Lceffler, 61. 

mallei (glanders), 84. 

tetanus, 80. 

typhosus, 25. 
Barlow's disease, 342. 
Basedow's disease, 345. 
Basophiles, 325. 

Baths in treatment of fever, 23. 
Bednar's aphthae, 233. 



Beef tape worm, 492. 

Bell's palsy, 370. 

Beri-beri, 437. 

Big-jaw (see Actinomycosis), 86. 

Bile in urine, 200 

Gmellin's test for, 201. 

Bile-passages, diseases of, 304, et seq, 

Biliary colic, 308, 309. 

Biliary fistula, 310. 

Birth palsies, 411. 

Black death (see Plague), in. 

Bladder, inflammation of (see 
Cystitis), 227. 

" Black measles," 72. 

" Black smallpox," 75. 

" Blasts," 323. 

Bleeder's disease, 339. 

Blepharospasm, 465. 

Blindness, word, 363, 364. 

Blood casts in urine, 208. 

Blood, coagulation, time of, test for, 
322. 

Blood corpuscles in urine, 205. 

Blood corpuscles, method of count- 
ing, 325- 

Blood, diseases of, 321. 

examination of, 321. 
specimen of, how to secure, 
322. 

Blood flukes, 494. 

Blood, fresh, microscopic appearance 
of, 322. 

Blood in feces, 248. 

Blood in stomach contents, test for, 

245- 

Blood in urine, 200, 205. 

Blood spitting (see Hemoptysis) , 174. 

Blood, stained, microscopic examina- 
tion of, 323. 

Blood vessels, diseases of, 140. 

Blue line on gums, 486. 

Bothriocephalus latus, 492. 

Bowel, affections of (see Intestines), 
266 et seq. 



500 



INDEX. 



Bradycardia, 137. 

Brain abscess, 407. 

Brain, diseases of, 391. 

Break-bone fever, 37. 

Breakfast, test, 242. 

"Brick-dust deposit" in urine, 202. 

Bright 's disease, classification of, 210. 

Bromatotoxismus, 488. 

Bronchial Catarrh (see Bronchitis) 

164. 
Bronchial flukes, 494. 
Bronchial glands, tuberculosis of, 

92. 
Bronchial tubes, diseases of, 164. 
Bronchiectasis, 169. 
Bronchitis, 164. 

acute simple, 165. 

capillary, 166. 

chronic, 168. 

plastic, 169. 
Bronchocele, 344. 
Bronchophony, 164. 
Bronchorrhea, 168. 
Brown atrophy of the heart, 136. 
Bubonic plague, in. 
Bulbar paralysis, 410. 



Cachexia, malarial, 49. 
Cachexia strumipriva, 347. 
Caisson disease, 435. 
Calcium oxalate in urine, 195, 203. 
Calculi, biliary, 308. 
Calculi, pancreatic, 316. 
Calculi, renal, 222. 
Cancer, intestinal, 280. 

of gall-ducts, 312. 

of liver, 302. 

of pancreas, 316. 

of stomach, 256. 
Cancrum oris (see Gangrenous stom- 
atitis), 233. 
Caput Medusae, 288, 297. 
Carbonates in urine, 198. 



Cardiac dulness, deep, 116. 

superficial, 116. 
Cardiac murmurs, 117. 
Cardialgia, 263. 
Caries of nasal bones, 151. 
Casts in urine, 206. 
Catalepsy, 472. 
Catarrh, chronic nasal, 151. 

chronic gastric, 250. 

suffocative, 166. 
Catarrhal croup, 153. 
Catarrhal dysentery, 43. 
Catarrhal fever (see Influenza), 40. 
Catarrhal gastritis, chronic, 250. 
Catarrhal jaundice, 307. 
Catarrhal nephritis, 211, 213. 
Catarrhal pharyngitis, 236. 
Catarrhal tonsillitis, 235. 
Cavities, pulmonary, signs of, 100. 
Central myelitis, 421, 
Central scotoma, 366. 
Cerebellar ataxia, 383. 
Cerebellar ataxia, hereditary, 429. 
Cerebellar hemorrhage, 400. 
Cerebral anemia, 396. 

apoplexy, 398. 

embolism, 402. 

hemorrhage, 398. 

hyperemia, 397. 

localization, 390. 

softening, 402. 

thrombosis, 402. 

paralysis, infantile, 411. 

syphilis, 441. 

tumor,. 404. 

type of paralysis, 379. 

typhus, 33. 
Cerebro-spinal fever, 53. 
Cerebro-spinal meningitis, epidemic 

(see Cerebro-spinal Fever), 53. 
Cervical myelitis, 422. 

pachymeningitis, 416. 
Cestodes, 491. 
Chancre, 105. 



INDEX. 



501 



Characteristic signs of infectious dis- 
eases, 22. 
Charcot's joints, 431. 
Charcot-Marie type of muscular atro- 
phy, 425- 
Cheese-cloth bath in infectious dis- 
ease, 24. 
Cheyne-Stokes respiration, 159. 
Chickenpox (see Varicella), 77. 
Children, diarrheas of, 268. 
Chloralism, 485. 
Chlorides in urine, 198. 
Chlorosis, 332. 
Chlorosis, Egyptian, 496. 
Choked disc, 405. 
Cholangitis, catarrhal, 310. 
Cholecystitis, suppurative, 308. 
Cholelithiasis, 308. 
Cholera Asiatica (see Asiatic Chol- 
era), 59. 
Cholera infantum, 268. 

morbus, 268. 

nostras, 268. 

sporadic, 268. 
Cholerine, 59. 
Chorea, 456. 

electrical, 460. 

grave, 457. 

gravidarum, 457. 

habit, 460. 

hereditary, 459. 

Huntingdon's, 459. 

minor, 456. 

of pregnancy, 457. 

paralytic, 457. 
Choreic movements, 385. 
Choreic status, 457. 
Choreiform diseases, 459. 
Chvostek's sign in tetany, 459. 
Chyluria, 195, 496. 
Circulatory system. 113. 

diseases of, 113. 
physical examination of, 
114. 



Circulatory symptoms referable to, 

113. 

Cirrhosis of the liver, 295. 

Claw-hand, 424. 

Clinical aspects of infectious disease, 
20. 

Clonic spasm, 383. 

Clonus, ankle, 389. 

Coagulation time of blood, test for, 
322. 

Cocainism, 486. 

Cold bath in infectious disease, 24. 

Cold compresses in infectious dis- 
eases, 24. 

Cold in the head, 150. 

Cold pack in infectious disease, 24. 

Colic, biliary, 308, 309. 

gall-stone, 308, 309. 
lead, 486. 
pancreatic, 316. 
renal, 223. 

Collapse, 21. 

Collapse of the lung, 181. 

Colles' law, 104. 

Color blindness, 366. 

Combined acids in stomach contents, 
test for, 244. 

Combined sclerosis, 427. 

Comma bacillus, 59. 

Common sensibility, tests of, 385. 

Concentric contraction of visual field, 
366. 

Congenital torticollis, 465. 

Congestion of the lungs, 172. 

Conjugate deviation of the eyes, 368. 

Conjunctival reflex, 387. 

Constipation, 279. 

Constitutional diseases, 349. 

Consumption (see Tuberculosis), 87, 
et seq. 

Contagious diseases, 17. 

Contagion, 17. 

Continued fever, 20. 

Contracted kidneys, 215. 



502 



INDEX. 



Contraction of visual field, concen- 
tric, 365. 
Contractures, 379, 383. 
Convalescence from infectious dis- 
ease, 25. 
Convalescence from typhoid, 33. 
Convergence, optic, defective, 367. 
Convulsion, 384. 
Convulsions, epileptic, 449. 

hysterical, 445. 

infantile, 469. 

Jacksonian, 385. 
Co-ordination, muscular, tests of, 

383. 
Coprolalia, 465. 
Corrigan's pulse, 128. 
Coryza, 150. 
Counting the red corpuscles, method 

of, 325- 
Coup de soleil, 473. 
Course of fever, 21. 
Cracked-pot sound, 161. 
Cramp, 383. 
Cramp, writer's, 462. 
Cranial nerve functions, 365. 
Cretinism, 347. 
Cremasteric reflex, 387. 
Crisis, 21. 

Crises, tabetic, 431. 
Crossed amblyopia, 365. 
Crossed diplopia, 367. 
Croup, catarrhal, 153. 
false, 153. 
membranous (see Diphtheria) 

62. 
spasmodic, 153. 
Croupous bronchitis (see Plastic 

Bronchitis), 169. 
Croupous pneumonia (see Pneumonic 

Fever), 55. 
Cuirass, tabetic, 431. 
Cutaneous reflexes, 387. 
Cylindroids in urine, 208. 
Cysticercus, 491, 492. 



Cystin in urine, 203. 
Cystitis, 227. 

Dandy fever, 37. 
Deafness, nerve, 37 1. 
Deafness, word, 363, 364. 
Deep reflexes, 388. 
Defervescence of fever, 21. 
Degenerations of the heart muscle, 

135. 

Degeneration, reaction of, 382. 

Delayed sensation, 387. 

Delirium cordis, 138. 

Delirium tremens, 483. 

Dementia, paralytic, 412. 

Dengue, 37. 

Derbyshire neck, 344. 

Desquamative nephritis, 211, 213. 

Diabetes insipidus, 352. 

Diabetes mellitus, 349. 

Diabetes, pancreatic, 350. 

Diabetic tabes, 350. 

Diacetic acid in urine, 201. 

Diagnosis of infectious disease, 21. 

Diaphragmatic movements, observa- 
tion of, 159. 

Diarrhea (see Enteritis), 265, 267. 

Diarrheas of children, 268. 

Diastolic shock in aortic aneurism, 

143. 

Diathesis, gout} T , 354. 
Diazo-reaction, 30. 
Diet in infectious disease, 23. 
Differential count of leucocytes, how 

made, 325. 
Diffuse myelitis, 421. 
Diffuse nephritis, 211, 213. 
Digestive tract, diseases of, 231. 
Digiti mortui, 467. 
Dilatation of the bronchial tubes (see 

Br 071 ch ie etas is ) , 169. 
Dilatation of the heart, 133. 
Dilatation of the stomach, 258. 
Diphtheria, 61. 



INDEX. 



503 



Diphtheritic dysentery, 43. 
Diphtheritic paralysis, 62. 
Diplegia, lesions causing, 380. 
Diplopia, 367. 

Disinfection in infectious disease, 23. 
Disseminated cerebro-spinal sclerosis, 

414. 
Dissociation, syringomyelic, 434. 
Distoma hematobium, 494. 

hepaticum, 493. 

pulmonalis, 494. 
Diver's paralysis, 435. 
Dreams, 472. 

Dropsy, abdominal {Ascites), 285. 
Dropsy, cardiac, treatment of, 131. 
Dropsy of gall-bladder, 308. 
Drug-habits (see Intoxications), 483. 
Dubini's disease, 460. 
Ductless glands, diseases of, 343. 
Dust, conveyance of infection by, 

18. 
D3'sarthria, 363. 
Dyschromatopsia, 444. 
Dysentery, 43. 
Dyspepsia, atonic, 261. 
Dyspepsia, nervous, 261. 
Dystrophy, muscular, 480. 

Echinococcus, 492. 
Eclampsia, infantile, 469. 
Ecstacy, 472. 

Edema, angioneurotic, 468. 
Edema glottidis, 154. 
Edema of the lungs, 173. 
Egyptian chlorosis, 496. 
Ehrlich's diazo-reaction, 30. 
Elbow jerk, 388. 
Electrical chorea, 460. 
Electrical irritability, method of test- 
ing, 381. 
Elephantiasis, 496. 
Embolism, cerebral, 402. 
Embryocardia, 138. 
Emotional condition, 363. 



Emphysema, 175. 

Emprosthotonos, 8t. 

Empyema (see Pleurisy, purulent), 

183. 
Empyema of gall-bladder, 30S. 
Encephalitis, acute hemorrhagic, 

407. 
Encephalitis, purulent, 407. 
Encephalopathy, lead, 487. 
Endarteritis, 140. 
Endocarditis, 123. 

chronic, 124. 

infective, 124. 

mural, 123. 
Endocardium, diseases of , 123. 
Enteralgia, 281. 

Enteric fever (see Typhoid), 25. 
Enteritis, acute, 265. 

chronic, 267. 
membranous, 281. 
Entero-colitis in children, 268. 
Enteroptosis, 263. 
Enumeration of blood corpuscles, 

325- 
Enuresis, 228. 
Eosinophiles, 324. 

Epidemic parotitis see Mumps), 79. 
Epigastric reflex, 3S7. 
Epilepsy, 449. 

nocturnal, 450. 

psychical, 450. 
Epithelial casts in urine, 207. 
Erb's phenomenon in tetany, 459. 
Erysipelas, 63. 
Erythrocytes, 322. 
Erythromelalg ; a, 437. 
Esophagitis, 238. 
Esophagus, diseases of, 238. 
stenosis of, 238. 
stricture of, 238. 
Estivo-autumnal malarial fever, 47. 
Exhaustion, heat, 472. 
Exhaustion, nervous, 453. 
Exophthalmic goitre, 345. 



504 



INDEX. 



External anthrax, 82. 
Eyes, conjugate deviation of, 368. 
motor nerves of, 366. 

Facial hemiatrophy, 469. 

Facial nerve, 370. 

Facial tic, 465. 

False casts in urine, 208. 

Famine fever (see Relapsing fever), 

36. 
Farcy (see Glanders), 84. 
Fastigum of fever, 21. 
Fatigue neurosis, 462. 
Fatty degeneration of the heart, 135. 
Fatty liver, 302. 
Fatty stools, 247, 305, 314. 
Fecal impaction, 272. 
Feces, examination of, 246. 
Feces, microscopical examination of, 

248. 
Fermentation test for sugar, 200. 
Ferrocyanic test for albumin, 199. 
Fetal rhythm, 138. 
Fever, 20. 

cheese cloth bath in, 24. 

cold bath in, 24. 

cold compress in, 24. 

cold pack in, 24. 

convalescence from, 25. 

diet in, 23. 

general treatment of, 23. 

hydrotherapy in, 23. 

inflammatory, 21. 

sponge bath in, 23. 

stimulants in^ 24. 

types of, 20. 
Fibrillation, 384. 
Fibrinous bronchitis (see Plastic 

Bronchitis'), 169. 
Fibrosis, arterio-capillary, 140. 
Field of vision, method of testing, 

365. 
Fifth nerve, diseases of, 368. 
Filaria sanguinis hominis, 496. 



First nerve, 365. 

Fish tape-worm, 492. 

Fish, poisoning by, 488. 

Fistula, biliary, 310. 

Flaccid paralysis, 379. 

Floating kidney, 226. 

Floating spleen, 319. 

Florid phthisis, 95. 

Flukes, 493. 

Follicular pharyngitis, 237, 

Follicular tonsillitis, 234. 

Fomites, 17. 

Food-poisoning, 488. 

Foreign bodies in the nose, 151. 

Formication, 387. 

Fremitus, vocal, 160. 

Friction, pericardial, 121. 

perihepatic, 289. 

pleural, 184. 
Friedlander's bacillus, 55. 
Friedreich's ataxia, 429. 
Fulgurant pains. 431. 
Functional nervous diseases, 442. 
Funnel-breast, 157. 

Gall-bladder, dropsy of, 308. 
Gall-bladder, empyema of, 308. 
Gall-ducts, cancer of , 312. 

diseases of, 286, et seq. 
parasites in, 312. 
stenosis of, 312. 
Galloping consumption, 95. 
Gallop rhythm, 138. 
Gall-stone colic, 308, 309. 
Gall-stones, 308. 
Gangrene of the lungs, 179. 
Gangrene, symmetrical, 467. 
Gangrenous stomatitis, 233. 
Gastralgia, 263. 
Gastric cancer, 256. 

catarrh, chronic, 250. 

dilatation, 258. 

neurasthenia, 261. 

neuroses, 260. 



INDEX. 



505 



Gastric ulcer, 253. 
Gastritis, acute, 249. 

acute toxic, 250. 

chronic catarrhal, 250. 

phlegmonous, 250. 
Gastrodynia, 263. 
Gastro-intestinal diseases, 239. 
Gastroptosis, 263. 
General management of fevers, 23. 
General paralysis of the insane, 412. 
General tuberculosis, 89. 
German measles (see Rubella) , 73. 
Girdle sensation, 421, 431. 
Glanders, 84. 
Glenard's disease, 263. 
Glossitis, 233. 

Glossopharyngeal nerve, 372. 
Gluteal reflex, 387. 
Glycosuria, 199. 

alimentary, 350. 
lipogenic, 350. 
Gmellin's test for bile, 201. 
Goitre, 344. 

exophthalmic, 345. 
Gout, 353. 

Gout, rheumatic, 356. 
Gouty kidney (see Chronic Interstial 

Nephritis), 215. 
Gower's solution, 325. 
Grand mal epileptique, 449. 
hysterique, 445. 
Granular casts in urine, 207. 
Grandular kidney (see Chronic Inter- 
stial Nephritis), 215. 
Granular pharyngitis, 237. 
Gravel (see Nephrolithiasis) , 222. 
Grave's disease, 345. 
Gray hepatization, 57. 
Green sickness (see Chlorosis ), 332. 

Habit chorea, 460. 
Habit spasm, 460. 
Haines' test for sugar, 200. 
Hallucinations of smell, 365. 



Hay fever, 152. 

Headache, sick, 463. 

Heart, albuminoid degeneration of, 

135. 
amyloid degeneration of, 136. 
arhythmia of, 137. 
atrophy of, 136. 
dilatation of, 133. 
fatty degeneration of, 135. 
fatty infiltration of, 136. 
failure, in typhoid, treatment 

of, 33- . 

fibroid degeneration of, 135. 

hypertrophy of, 131. 

in rheumatic fever, 51. 

intermission of, 137. 

irregularity of, 137. 

neuroses of, 136. 

palpitation of, 136. 

physical examination of, 114. 

relative insufficiency of, 125. 

treatment of valvular disease 
of, 131. 

valvular disease, 125. 
Heat exhaustion, 472. 
prostration, 472. 
Heat-stroke, 473. 
Heat test for albumin, 199. 
Heberden's nodosities, 356. 
Heller's test for albumin, 199. 
Hematemesis, 259. 
Hematoma of the dura mater, 391. 
Hematuria, 200, 205. 
Hemianesthesia, hysterical, 444. 
Hemianopsia, 366. 
Hemiatrophy, facial, 467. 
Hemicrania, 463. 
Hemiplegia, 399. 

hysterical, 446. 
localization of lesion 
causing, 380. 
Hemiplegic state, 399. 
Hemoglobin, estimation of, 329. 
Hemoglobinuria, 200, 205. 



506 



INDEX. 



Hemoglobinuria, malarial, 48. 
Hemopericardium, 123. 
Hemophilia. 339. 
Hemoptysis, 174. 

treatment of, 104. 
Hemorrhage, cerebellar, 400. 

cerebral, 398. 

into stomach, 259. 

intracranial, 398. 

spinal, 418. 
Hemorrhagic diathesis, 339. 

encephalitis, acute, 

407. 
measles, 72. 

Hemosporidia, 45. 

Hemothorax, 189. 

Henoch's purpura, 340. 

Hepatic abscess, 43. 

intermittent fever, 310. 

Hepatitis, acute parenchymatous, 
300. 

Hepatitis, interstitial (see Cirrhosis 
of liver), 295. 

Hepatitis, suppurative, 293. 

Hepatoptosis, 263. 

Hereditary ataxia, 429. 

cerebellar, 429. 
chorea, 459. 
spastic paraplegia, 427. 

Hippocratic facies, 283. 

Hippuric acid, 197. 

History of previous infectious dis- 
eases, 21. 

Hodgkin's disease, 337. 

Homonymous diplopia, 367. 

Homonymous hemianopsia, 366. 

Huntingdon's chorea, 459. 

Hyaline casts in urine, 206. 

Hydatid cyst of the liver, 492. 

Hydatid thrill, 289. 

Hydrencephaloid, 395. 

Hydrocephaloid, 395. 

Hydrocephalus, 394. 



Hydrocephalus, acute {Meningeal 
tuberculosis) , 91. 
spurious, 395. 
Hydrochloric acid in stomach con- 
tents, test for, 243. 
Hydronephrosis, 224. 
Hydropericardium, 123. 
Hydrophobia (see Rabies), 83. 
Hydro-pneumothorax, 188. 
Hydrops vesicae felleae, 308. 
Hydrotherapy in treatment of infec- 
tious disease, 23. 
Hydrothorax. 189. 
Hyperacidity, 262. 
Hyperacusis, 371. 
Hyperalgesia, tests for, 386. 
Hyperchlorhydria, 262. 
Hyperemia, cerebral, 397. 

of the lungs, 172. 
Hyperesthesia, auditory, 371. 

cutaneous, examina- 
tion for, 386. 
hysterical, 445. 
Hyperleucocytosis, 327. 
Hyperosmia, 365. 
Hyperpyrexia, 21. 

in rheumatic fever, 51. 
Hypertrophic pharyngitis, 237. 

rhinitis, 151. 
Hypertrophy of the tonsils, 235. 
Hypochondriasis, 454. 
Hypoglossal nerve, 373. 
Hypoleucocytosis, 328. 
Hysteria, 442. 

convulsions in, 445. 

major, 445. 

minor, 445. 

motor phenomena in, 446. 

paroxysmal phenomena of, 

445- 
traumatic, 464. 
Hysterical abdomen, 284. 
amblyopia, 366. 
convulsions, 445. 



INDEX. 



507 



Hysterical hemiplegia, 446. 

monoplegia, 446. 

paralysis, 446. 

rhythmical spasms, 447. 

tics, 447. 

tremors, 447. 
Hysterogenic zone, 445. 



Icterus, 304. 

neonatorum, 306. 
gravis, 300. 
saturninus, 486. 
Ileus [Intestinal Obstruction) , 271. 
Immunity, 18. 

acquired, 18. 
experimental, 18. 
natural, 18. 
Impaction, fecal, 272. 
Incontinence of urine, 228. 
In co-ordination, 383. 
Incubation, period of, 19. 
Incubus, 472. 
Indican, 197. 
Indigestion, intestinal, in children, 

268. 
Infantile cerebral palsies, 411. 
convulsons, 469. 
eclampsia, 469. 
form of muscular dys- 
trophy, 481. 
Infected patient, management of, 22. 
Infection, 17. 
Infectious diseases, 17. 

characteri stic 

signs of, 22. 
cleanliness in, 22. 
clinical aspects of, 

20. 
diagnosis of, 21. 
diet in, 23. 
disinfection in, 23. 
general manage- 
ment of, 22. 



Infectious diseases, general treatment 
of, 23. 
temperature in , 
21. 
Infectiousness, period of, 19. 
Inferior polioencephalitis, 410. 
Inflammatory^ fever, 20. 

rheumatism (see Rheu- 
matic Fever), 51. 
Influenza, 40. 
Insects, conveyance of infection by, 

18. 
Insolation, 473. 
Insomnia, 471. 
Insufficiency, aortic, 127. 
mitral, 125. 
pulmonic, 129. 
relative, 125. 
tricuspid, 129. 
Insular sclerosis, 4T4. 
Intellectual functions, examination 

of, 363- 
Intention tremor, 384. 
Intercostal myalgia, 1S6. 

neuralgia, 186. 
Interlobular emphysema, .175. 
Intermittent fever, 20. 

Charcot's, 310. 
malarial, 47. 
Intermittent fever, hepatic, 310. 
Internal anthrax, 82. 
Interstitial emphysema, 175. 
Interstitial hepatitis (see Cirrhosis of 
Liver), 295. 
cancer, 280. 
Intestinal hemorrhage, treatment 
of, 32. 
indigestion in children, 

268. 
mycosis(see/4«//2rfljr),82. 
nephritis, chronic, 215. 
nephritis, suppurative 
( see Pyeloneph ritis ) , 
219. 



508 



INDEX. 



Intestinal neuralgia, 281. 

neuroses, 281. 

obstruction, 271. 

perforation, in typhoid, 33 
Intestines, cancer of, 280. 
Intoxications, 483. 
Intracranial tumor, 404. 
Intussusception, 271. 
Invagination, 271. 

Invasion of the body by micro-organ- 
isms, 18. 
Irregular gout, 454. 

Jacksonian convulsions, 385. 
Jail fever, 33. 
Jaundice, 304. 

hepatogenous, 304. 

hematogenous, 305. 

in liver diseases, 287. 

in pyemia, 68. 

in relapsing fever, 37. 

in septicemia, 67. 

in yellow fever, 42. 

malignant, 300. 

simple catarrhal, 307. 
Jaw jerk, 388. 
Joints, Charcot's, 431. 
Jumpers, 466. 

Juvenile form of progressive muscu- 
lar dystrophy, 480. 

Kakke, 437. 

Kernig's sign of cerebro-spinal men- 
ingitis, 54. 
Kidney, amyloid, 218. 

congestion of, 209, 210. 

contracted, 215. 

floating, 226. 

gouty, 215. 

granular, 215. 

hyperemia of, 209, 210. 

inflammation of (see Ne- 
phritis). 

lardaceous, 218. 



Kidney, large white, 213. 

movable, 226. 

passive congestion of, 210. 

physical examination of, 
192. 

small white, 213. 

stone in the, 222. 

surgical Csee Pyelone- 
phritis), 219. 

tuberculosis of, 221. 

waxy, 218. 
Klebs-Lceffler bacillus, 6r. 
Knee jerk, 388. 
Koplik's sign of measles, 71. 
Kreatinin, 197. 

Labio-glosso-laryngeal paralysis, 410. 

Labryinthine vertigo, 371. 

Lactic acid in stomach-contents, test 

for, 244. 
Lsennec's cirrhosis of liver, 296. 
La Grippe (see Influenza), 40. 
Landouzy-Dejerinetype of muscular 

dystrophy, 481. 
Landry's paralysis, 419. 
Lardaceous kidney, 218. 
Lardaceous liver, 299. 
Large white kidney, 213. 
Laryngeal diphtheria, 62. 
Laryngitis, acute catarrhal, 153. 
chronic catarrhal, 154. 
edematous, 154. 
syphilitic, 155. 
tubercular, 155. 
Larynx, examination of, 149, 372. 
Latah, 466. 
Lateral sclerosis, 426. 

amyotrophic, 425. 
Lead colic, 486. 

encephalopathy, 487. 
neuritis, 437. 
palsy, 437. 
Lead-poisoning, 486. 
Leucin in urine, 204. 



INDEX. 



509 



Leucocytes in urine, 205. 

large mononuclear, 324. 
polynuclear, 324. 
small mononuclear, 324. 
varieties of, 324. 
Leucocythemia, 334. 
Leucocytosis, 327. 

in malaria, 49. 
in pneumonia, 56. 
in rheumatic fever, 52. 
in typhoid, 33. 
Leucopenia, 328. 
Leukemia, 334. 

lymphatic, 335. 
spleno-medullary, 335. 
Lepra, 109. 
Leprosy, 109. 

anesthetic, no. 
tubercular, no. 
Leptomeningitis, 392, 417. 
Lightning pains, 431. 
Light, reaction to, 368. 
Lipogenic glycosuria, 350. 
Lithemia (see Irregular gout), 354. 
Lithiasis, biliary, 308. 

renal, 222. 
Little's disease, 412. 
Liver, abscess of, 293. 

acute yellow atrophy of, 300. 
albuminoid, 299. 
amyloid, 299. 
anemia of, 291. 
cancer of, 302. 
cirrhosis of, 295. 
congestion of, 291. 
cyanotic atrophy of, 291. 
diseases of, 286, et seq. 
examination of, 288. 
fatty degeneration of, 302. 
fatty infiltration of, 302. 
flukes, 493. 
hydatid cyst of, 492. 
hyperemia of, active, 291. 
passive, 291. 



Liver, lardaceous, 299. 

malformations of, 290. 
malpositions of, 290. 
" nutmeg," 291. 
percussion limits of, 290. 
red atrophy of, 291. 
wandering, 293. 
waxy, 299. 
Lobar pneumonia (see Pneumonic 

Fever), 55. 
Local asphyxia, 467. 
Local syncope, 467. 
Localization, cerebral, 390. 
Lockjaw (see Tetanus), 80. 
Locomotor ataxia, 430. 
Lower neuron, 378. 
Lower respiratorv tract, diseases of, 

156. 
Lower respiratory tract, examination 

of, 157. 
Lues venerea (see Syphilis), 104. 
Lumbago, 479. 
Lumbar puncture, in cerebro-spinal 

fever, 54. 
Lumpy jaw (see Actinomycosis), 86. 
Lungs, abscess of, 180. 

congestion of, 172. 
consumption of the, 93. 
edema of, 173. 
gangrene of, 179. 
hyperemia of, 172. 
tuberculosis of the, 93. 
tumors of, 181. 
Lymphadenitis, tuberculous, 92. 
Lymphatic leukemia, 335. 
Lymphemia, 335. 
Lympho-sarcoma, 337. 
Lyssa (see Rabies), 83. 

Macrocytes, 322, 
Main en griffe, 424. 
Malacosteon, 359. 
Malaria, 45. 

malignant, 47. 



510 



INDEX. 



Malarial parasite, 45. 

paroxysm, 46. 
Malignant jaundice, 300. 
Malignant malaria, 47. 
Malignant measles, 72. 
Malignant pustule (see Anthrax), 

82. 
Management of an infected patient, 

22. 
Management of fevers, 23. 
Mania a potu, 483. 
Markzellen, 324. 
Mayo-Robson point, 310. 
McBurney's point, 276. 
Measles, 71. 

Melsena neonatorum, 260. 
Melasma, 343. 

Membranous bronchitis, 169. 
Membranous croup, 62. 
Membranous enteritis, 281. 
Meniere's disease, 371. 
Meningitis, epidemic cerebro-spinal, 

53 
Meningeal tuberculosis, 91. 
Meningitis, basilar, 91. 

cerebral, 391. 

spinal, 416. 

tubercular, 91. 
Meningococcus intracellularis, 53. 
Mental condition, examination as to, 

363. 
Mental torticollis, 466. 
Metallic tinkling, 164. 
Metastatic abscesses, 67. 
Metatarsalgia, 440. 
Micrococcus lanceolatus, 55. 
Microcytes, 322. 
Micro-organisms, methods of access 

to body, 18. 
Microscopical examination of urine, 

201. 
Migraine, 463. 
Miliary fevei, 39. 
Miliary tuberculosis, 89. 



Miliary tuberculosis of the intes- 
tines, 89. 
of the lungs, 

9°. 93- 
of the men- 
inges, 91. 
Milk, conveyance of infection by, 17. 
Mimic spasm, 465. 
Mitral area, auscultation of, 116. 

insufficiency, 125. 

obstruction, 126. 

regurgitation, 125. 

stenosis, 126. 
Mollifies ossium, 359. 
Monoplegia, hysterical, 446. 
Monoplegia, localization of lesions 

causing, 380. 
Morbilli (see Measles), 71. 
Morbus Weilhofii, 340. 
Morphinism, 4S5. 
Morvan's disease, 434. 
Motor aphasia, 364. 
Motor ataxia, 383. 

Motor functions, examination of, 374. 
Motor function of stomach, test for, 

245. 
Motor nerves of eye, 366. 
Motor phenomena in hysteria, 446. 
Mouth, affections of , 231. 

examination of, 231. 
Movable kidney, 226. 
Multiple abscesses, 67. 
Multiple sclerosis, 414. 
Multiple neuritis, 436. 
Mumps, 79. 

Muscles, diseases of the, 477. 
Muscular atrophy, progressive, 

spinal, 424. 
Muscular co-ordination, tests of, 383. 
Muscular cramps, 486. 
Muscular dystrophy, 480. 
Muscular movements, abnormal, 383. 
Muscular nutrition, tests of, 381. 
Muscular power, tests of, 374. 



INDEX. 



511 



Muscular rheumatism, 479. 

Muscular sense, tests of, 386. 

Myalgia, 479. 

Mycosis, intestinal (see Anthrax) ,82. 

Myelitis, 420. 

Myelitis, acute polio-, 423. 

cervical, 422. 

chronic, 422. 
Myelocytes, 324. 
Myocarditis, acute, 134. 

chronic, 135. 
fibrous, 135. 
Myocardium, diseases of, 131. 
Myoclonus, 460. 
Myopathic facies, 481. 
Myositis, 477. 

ossifying, 478. 

primary, 477. 

rheumatic, 479. 

secondary, 478. 
Myotonia congenita, 479. 
Myotonic reaction, 480. 
Myriachit, 466. 
Myxedema, 347. 

operative, 347. 



Narcolepsy. 472. 

Nasal catarrh, acute, 150. 

chronic, 151. 
Nasal diphtheria, 62. 
Necrosis of nasal bones, 151. 
Nematodes, 494. 
Nephritis, acute parenchymatous, 

211. 
Nephritis, ascending, 219. 

catarrhal, 21 t, 213. 

chronic interstitial, 215. 

chronic parenchymatous, 
213. 

desquamative, 211, 213. 

diffuse, 211, 213, 

obstructive, 219. 

parenchymatous, 211, 213. 



Nephritis, suppurative, 219. 

tubal, 211, 213. 
Nephritides (see B sight's Disease), 

210. 
Nephrolithiasis, 222. 
Nephroptosis, 226, 263. 
Nerve deafness, 371. 
Nerves, cranial, functions of, 365. 
Nerves, peripheral, diseases of, 435. 
Nervous diarrhea, 281. 
Nervous diseases, functional, 442. 
Nervous dyspepsia, 261. 
Nervous exhaustion, 453. 
Nervous prostration, 453. 
Nervous system, diseases of, 361. 

examination of, 362. 
syphilis of, 440. 
Neuralgia, 439. 

of the bowel, 281. 
of the heart {see Angina 
pectoris), 138. 
Neuralgia of the stomach, 263. 
Neurasthenia, 453. 

gastric, 261. 
traumatic, 464. 
Neuritis, 435. 

alcoholic, 437. 
arsenical, 488 
lead, 437, 486. 
multiple, 436. 
simple, 436. 
Neuron, lower, 378. 
upper, 378. 
Neuroses, 442. 

fatigue, 462. 
intestinal, 281. 
occupation, 462. 
traumatic, 464. 
Neutrophil es, 325. 

polynuclear, 324. 
Night-mare, 472. 
Night-terrors, 472. 
Nitric acid test for albumin, 199. 
Nocturnal epilepsy, 450. 



512 



INDEX. 



Nodosities, Heberden's, 356. 

Noma (see Gangrenous Stomatitis), 

233- 
Normal temperature, 22. 
Nose, diseases of, 150. 

examination of, 148. 
Nuclear ophthalmoplegia, 408. 
Nutmeg liver, 291. 
Nystagmus, 368, 384. 

Obesity, 359. 
Obstruction, aortic, 128. 

intestinal, 271. 

mitral, 126. 

pulmonic, 129. 

pyloric, 258. 

tricuspid, 129. 
Obstructive nephritis (see Pyelo- 
nephritis), 219. 
Occupation neuroses, 462. 
Olfactory nerve, 365. 
Omalgia, 479. 
Onset of infectious disease, mode of, 

21. 
Operative myxedema, 347. 
Ophthalmoplegia, nuclear, 408. 
Opisthotonos, 81. 
Optic nerve, 365. 
Optic neuritis, due to intracranial 

tumor, 405. 
Orchitis, complicating mumps, 80. 
Organic acids in stomach contents, 

test for, 244. 
Organic reflexes, 389. 
Ossifying myositis, 478. 
Osteoarthritis, 356. 
Osteomalacia, 359. 
Osteophytes, 356. 
Ovarian cyst, 285. 
Oxyphiles, 325. 
Oxyuris vermicularis, 494. 
Ozsena, 151. 

Pachymeningitis, cerebral, 391. 
spinal, 416. 



Pain, hepatic, 286. 
Pain sense, tests of, 386. 
Pains, fulgurant, 431. 
lightning, 431. 
Palatal reflex, 387. 
Palpitation of heart, 136. 
Palsy, Bell's, 370. 

shaking, 460. 
Pancreas, diseases of, 314. 

examination of, 314, 
Pancreatic calculi, 316. 
cancer, 316. 
colic, 316. 
cysts, 316. 
diabetes, 350. 
Pancreatitis, acute, 314. 

chronic, 316. 
gangrenous, 315. 
hemorrhagic, 315. 
suppurative, 315. 
Paragraphia, 364. 
Paralysis, 375, et seq. 

acute ascending, 419. 

agitans, 460. 

atrophic spinal, 423. 

bulbar, 410. 

cerebral type of, 379. 

diver's, 435. 

general, of the insane, 

412. 
hysterical, 446. 
infantile cerebral, 411. 
infantile spinal, 423. 
labio-glosso-lary ngeal ,410. 
Landry's, 419. 
laryngeal, 373. 
localization of lesion caus- 
ing, 380. 
pseudo-hypertrophic, 480. 
spastic spinal, 426. 
spinal type of, 379. 
Paralytic chorea, 457. 
Paralytic dementia, 412. 
Paralytic strabismus, 367. 



INDEX. 



513 



Paralytic thorax, 157. 
Paramimia, 365. 
Paramyoclonus multiplex, 460. 
Paraphasia, 364. 
Paraplegia, spastic, 426. 

spastic, hereditary, 427. 
Parasites, animal, diseases due to, 491. 
Parasyphilitic lesions, 440. 
Parenchymatous nephritis, 211, 213. 
Paresis, general, 412. 
Paresis, muscular, 374. 
Paresthesia, 386. 
Paris Green, poisoning by, 487. 
Parkinson's disease, 460. 
Parosmia, 365. 

Parotitis, epidemic (see Mumps), 79. 
Paroxysmal phenomena of hysteria, 

445- 
Passive tremor, 384. 
Pavor nocturnus, 472. 
Peliosis rheumatica, 51, 340. 
Pelvic affections in women, 277. 
Perforation, intestinal, in typhoid, 

33- 
Pericarditis, 121. 
Pericardium, diseases of, 121. 
Perihepatitis, 292. 
Perinephritic abscess, 277. 
Period of incubation, 19. 
Period of infectiousness, 19. 
Peripheral nerves, diseases of, 435. 
Perisplenitis, 317. 
Peritoneum, diseases of, 282. 
Peritonitis, acute, 2S2. 

acute circumscribed, 283. 

chronic, 284. 
Pernicious anemia, 333. 
Pernicious malaria, 47. 
Peroneal type of, muscular atrophy, 

425- 
Pertussis (see Whooping Cough), 78. 
Petit mal, 450. 
Pfeiffer's bacillus, 40. 
Phagocytosis, 18. 

33 



Pharyngitis, atrophic, 237. 

catarrhal, 237. 

follicular, 237. 

granular, 237. 

hypertrophic, 237. 

phlegmonous, 237. 

sicca, 237. 

ulcerative, 237. 
Pharynx, examination of, 149, 232, 

372. 
Phlegmonous pharyngitis, 237. 
Phlegmonous tonsillitis, 235. 
Phosphates in urine, 195, 198, 204. 
Phosphorus-poisoning, 301. 
Phthisis Florida, 95. 

pneumonic, 95. 
pulmonalis (see Pulmonary 

tuberculosis), 93, et seq. 
Physical examination in infectious 

diseases, 21. 
Physical examination of the respira- 
tory organs, 157. 
Physiological albuminuria, 198. 
Picric acid test for albumin, 199. 
Pigeon-breast, 157. 
Pin worm, 494. 
Plague, in. 
Plantar reflex, 387. 
Plasmodium malarise, 45. 
Plastic bronchitis, 169. 
Pleurisy, 183. 

Pleuritic effusion, 183, et seq. 
Pleuritis (see Pleurisy) , 183. 
Pleurodynia, 479. 
Pleuro-pneumonia, 57. 
Pleurosthotonos, 81. 
Plumbism, 486. 
Pneumococcus, 55. 
Pneumogastric nerve, 372. 
Pneumonia (see Pneumo7iic Fever), 

55- 
aspiration, 177. 
broncho-, 177. 
catarrhal, 177. 



514 



INDEX. 



Pneumonia, croupous (see Pneumonic 
Fever), 55. 
lobar (see Pneumonic 

Fever), 55. 
lobular, 177. 
Pneumonic fever, 55. 
Pneumopericardium, 123. 
Pneumo-thorax, 187. 
Pock marks, 75, 
Podagra (see Gout), 353. 
Poikilocytes, 322. 
Poisoning, arsenical, 187. 
food, 488. 
lead, 486. 
phosphorus, 301. 
ptomaine, 488. 
strychnine, 81. 
Polioencephalitis, superior acute, 408. 
chronic, 409. 
Polioencephalitis, inferior, 410. 
Polioencephalomyelitis, 410. 
Poliomyelitis anterior, acute, 423. 

chronic, 424. 
Poliomyositis, acute infectious, 477. 
Polyneuritis, 436. 
Polysarcia, 359. 
Polyuria, simple, 353. 
Porencephalus, 411. 
Pork tape-worm, 491. 
Portal vein, diseases of, 313. 

thrombosis of, 313. 

septic of, 313. 
Post-diphtheritic paralysis, 62. 
Postero-lateral sclerosis, 427. 
Post-malarial anemia, 49. 
Pott's disease, 157. 
Pox (see Syphilis), 104. 
Pregnancy, chorea of, 457. 

extra-uterine, 278. 

Pressure sense, tests of, 386. 
Progressive muscular atroph}', spinal, 

424. 
Progressive spastic ataxia, 427. 



Prophylaxis against Asiatic cholera, 
60. 

Prophylaxis against infectious dis- 
eases, 2?. 

Prophylaxis against typhoid fever, 

31. 
Prophylaxis against typhus fever, 35. 
dysentery, 44. 
malarial fevers, 

50. 
rabies, 84. 
tuberculosis, 101. 
whooping cou gh 

79- 
Propulsion, 461. 
Prostration, heat, 472. 
Prostration, nervous, 453. 
" Prune-juice " sputum, 55. 
Pruritus, 387. 

Pseudo-hypertrophic paralysis, 480. 
Pseudo-leukemia, 337. 
Pseudo-tabes, 437. 
Psychical epilepsy, 450. 
Ptomaine-poisoning, 488. 
Pulmonary abscess, 180. 

congestion, 172. 

edema, 173. 

gangrene, 179. 

hyperemia, 172. 

tuberculosis, 93. 

acute pneumonic, 94, 

95- 
broncho-pneumonic, 

95- 

caseous, 94, 95. 

fibroid, 94, 96. 

fibro-caseous, 94, 97. 

lobar, 96. 

miliary, 90, 93. 

prophylaxis of, 10 1. 
Pulmonic area, auscultation of, 117. 
insufficiency, 129. 
obstruction, 129. 
regurgitation, 129. 



INDEX. 



515 



Pulmonic stenosis, 129. 
Pulse, 119. 

Corrigan's, 128. 
trigeminal, 138. 
water-hammer, 128. 
Pulsus tardus, 128. 
Pupil, Argyll-Robertson, 368, 431. 
Pupillary- skin reflex, 387. 
Pupils, examination of, 368. 
Purpura, 340. 

arthritic, 340. 

hemorrhagica, 340. 

Henoch's, 340. 

rheumatica, 340. 

secondary, 340. 

simple, 340. 
Purulent encephalitis, 407. 
Pus casts in urine, 208. 
Pus corpuscles in urine, 205. 
Pustule, malignant, 82. 
Pyelitis, 219. 
Pyelonephritis, 219. 
Pylephlebitis, adhesive, 313. 

suppurative, 294, 313. 
Pyloric obstruction, 258. 
Pyogenic infection, in diphtheria, 61. 
Pyonephrosis, 219, 225. 
Pyo-pneumothorax, 184, 188. 
Pyo-pneumothorax, subphrenic, 292. 
Pyrexia, 20. 
Pyuria, 205. 

Qualitative alterations in electrical 

irritability, 382. 
Quantitative alterations in electrical 

irritability, 382. 
Quantitative estimation of albumin, 

199. 
Quantitative estimation of sugar, 200. 
Quartan malarial fever, 47. 
Quinsy, 235. 
Quotidian malarial fever, 47. 

Rabies, 83. 



Rachitic rosary, 157, 358. 

Rachitis, 358. 

Ray fungus, 86. 

Raynaud's disease, 467. 

Reaction of degeneration, 382. 

Reaction, myotonic, 480. 

Reactions, electrical, method of test- 
ing, 381. 

Recrudescence in typhoid, 29. 

Red corpuscles, 322. 

nucleated, 323. 

Red hepatization, 57. 

Reflexes, 3S7. 

Reflex functions, examination of, 387. 

Regular gout, 354. 

Regurgitation, aortic (see Aortic In- 
sufficiency), 127. 

Regurgitation, pulmonic, 129. 

Regurgitation, tricuspid, 129. 

Reichmann's disease, 262. 

Relapse in typhoid, 29. 

Relapsing fever, 36. 

Remittent fever, 20. 

Renal calculus, 222. 

Renal colic, 223. 

Renal hyperemia, 209, 210. 

Renal inflammation (see Nephritis) , 
210. 

Renal tuberculosis, 221. 

Resistance to infection, 18. 

Respiratory organs, examination of, 

157. 

Respiratory system, diseases of, 147. 
Respiratory tract, upper, diseases of, 

147. 
Results of testing functional activity 

of stomach, significance, 245. 
Retention of urine, 229. 
Retrocedent gout, 354. 
Retropharyngeal abscess, 238. 
Rheumatic fever, 51. 
Rheumatic gout, 356. 
Rheumatism (see Rheumatic Fever) , 

5i. 



516 



INDEX. 



Rheumatism, muscular, 479. 
Rheumatic myositis, 479. 
Rheumatic nodules, 51. 
Rheumatic purpura, 51. 
Rheumatoid arthritis, 356. 
Rhinitis, acute, 150. 

atrophic, 151. 

chronic, 151. 

chronic hypertrophic, 151. 
' ' Rice water ' ' stools in Asiatic 

cholera, 60. 
Rickets, 358. 
Romberg's sign, 430. 
Rose cold (see Hay fever) , 152. 
Rosenbach's reaction, 266. 
Rotheln (see Rubella), 73. 
" Rough on rats," poisoning by, 487. 
Rouleaux, 323. 
Round worm, 494. 
Rubella, 73. 

Rubeola (see Measles), 71. 
" Rusty " sputum, 55. 

Sapremia, 65. 
Saturnism, 486. 
Scapular reflex, 388. 
Scarlatina anginosa, 69. % 
Scarlatina (see Scar lei Fever), 68. 
simplex, 69. 

maligna, 69. 
Scarlet fever, 68. 

Scarlet rash (see Scarlet Fever), 68. 
Scleroderma, 468. 
Sclerosis, amyotrophic lateral, 425. 

combined, 427. 

disseminated, 414. 

insular, 414. 

lateral, 426. 

multiple, 414. 

of the posterior columns, 
430. 

postero-lateral, 427. 

posterior spinal, 430. 
Scorbutus, 341. 



Scotoma, central, 366. 
Scrofula, 92. 
Scurvy, 341. 

infantile, 342. 
Second nerve, 365. 
Sediments, urinary, 202. 
Senile tremor, 461. 
Sensory aphasia, 363. 

phenomena of hysteria, 447. 
Sepsis intestinalis, 65. 
Septicemia, 66. 
Septic fevers, 65. 

infection, 66. 

intoxication, 65. 

temperature, 68. 
Sexual neurasthenia, 454. 
Shaking palsy, 460. 
Ship fever, 33. 
Sick headache, 463. 
Signal symptom, 385. 
Sign, Romberg's, 430. 

Westphal's, 431. 
Simple neuritis, 436. 
Sleep, disorders of, 471. 
Small-pox (see Variola), 74. 
Small white kidney, 213. 
Smell, hallucinations of, 365. 
Softening, cerebral, 402. 
Somnambulism, 471. 
Sore throat (see Pharyngitis), 236, 

237. 
Spasm, 383. 

habit, 460. 

mimic, 465. 
Spasmodic croup, 153. 
Spasms, rhythmical, in hysteria, 447, 
Spasmodic strabismus, 367. 
Spastic ataxia, progressive, 427. 
Spastic paraplegia, 426. 

hereditary, 427. 
Spasticity, muscular, 379, 383. 
Specific lesions, 440. 
Speech, disturbances of, 363. 
Sphygmograph, 119. 



INDEX. 



517 



Spinal accessory nerve, 373. 
Spinal cord, diseases of, 416. 
Spinal curvature, 157. 

form of progressive muscular 
atrophy, 424. 

hemorrhage, 418. 

pachymeningitis, 416. 

leptomeningitis, 417. 

paralysis, spastic, 426. 

sclerosis, amyotrophic lateral, 

425. 
combined, 427. 
lateral, 426. 
posterior, 430. 
postero-lateral, 427. 
syphilis, 441. 
Spinal type of paralysis, 379. 
Spirillum fever (see Relapsing 

Fever), 36. 
Spirillum Obermeieri, 36. 
Spirocheta, 36. 
Splanchnoptosis, 263. 
Spleen, abscess of, 318. 
amyloid, 319. 
diseases of, 317. 
examination of, 317. 
floating, 319. 
inflammation of, 318. 
neoplasms of, 318. 
rupture of, 318. 
Splenic anemia, 336. 
Splenic fever (see Anthrax), 82. 
Splenitis, 318. 

Spleno-medullary leukemia, 335. 
Splenoptosis, 263. 
Spondylitis deformans, 158. 
Sponge baths in infectious disease, 

23- 
Spotted fever, 53. 
Spurious albuminuria, 198. 
Spurious torticollis, 466. 
Squint (see Strabismus) , 367. 
Stage of reaction in Asiatic cholera, 

60. 



St. Anthony's fire (see Erysipelas), 

63. 
State, typhoid, 2r. 
Static ataxia, 383. 
Status epilepticus, 450. 
Strangulation of bowel, 271. 
" Strawberry tongue," 69. 
Stellwag's sign, 346. 
Stenocardia (see Angina Pectoris), 

138. 
Stenosis, aortic, 128. 

of esophagus, 238. 
of gall-ducts, 312. 
mitral, 126. 
pulmonic, 129. 
tricuspid, 129. 
St. Gothard's disease, 496. 
Stigmata, hysterical, 443. 
mental, 445. 
motor, 445. 
sensory, 443. 
Stimulants in infectious disease, 24. 
Stomach and intestines, diseases of, 

239- 
Stomach, cancer of, 256. 
catarrh of, 250. 
dilatation of, 258. 
disorders, symptoms of, 

239- 
functional disorders of, 260. 
hemorrhage into, 259. 
neuralgia of, 263. 
neuroses of, 260. 
ulcer of, 253. 
Stomach- contents, withdrawal of, 

243. 
Stomach-contents, chemical exami- 
nation of, 243. 
Stomach-contents, examination of, 

243. 
Stomach, external examination of, 

241. 
Stomach functions, examination of, 

242. 



518 



INDEX. 



Stomatitis, 232. 

Stone in the kidney, 222. 

Stools, pathological, 247. 

color of, 247. 

consistence of, 247. 

microscopical examination 
of, 248. 

odor of, 248. 

abnormal constituents of, 
248. 
Strabismus, 367. 
Stricture of bowel, 271. 
Stricture of esophagus, 238. 
Strongylus duodenalis, 496. 
Struma, 344. 

Strychnine-poisoning, 81. 
St. Vitus' dance, 456. 
Sub-diaphragmatic abscess, 184, 292. 
Subphrenic abscess, 292. 
Subphrenic pyopneumothorax, 292. 
Suffocative catarrh (see Capillary 

Bronchitis), 166. 
Sugar in urine, 199. 

tests for, 199, 200. 
quantitative estimation of, 
200. 
Sulphates, in urine, 197, 198. 
Sunstroke, 472. 
Superficial reflexes, 387. 
Superior polioencephalitis, 408, 409. 
Suppression of urine, 229. 
Suppurative interstitial nephritis (see 

Pyelonephritis}, 219. 
Suppurative cholecystitis, 308. 
Suppurative pylephlebitis, 294. 
Suppurative tonsillitis, 235. 
Supra-renal capsule, diseases of, 343. 
Susceptibility, 18. 
Sweating sickness, 39. 
Sydenham's chorea, 456. 
Symmetrical gangrene, 467. 
Symptomatic anemia, 330. 
Symptomatic torticollis, 465. 
Symptom, signal, 385. 



Syncope, local, 467. 
Syphilis, 104. 

acquired, 105. 

cerebral, 441. 

hereditary, 107. 

of the larynx, 155. 

of the nervous system, 440. 

spinal, 441. 
Syphilitic cirrhosis of liver, 296. 
Syringomyelia, 433. 
Syringomyelic dissociation, 434. 

Tabes dorsalis, 430. 

Tabes mesenterica, 93. 

Tabetic crises, 431. 

Tabetic cuirass, 431. 

Tabetic ulcer, 432. 

Tache cerebrale, 393. 

Tachycardia, 137. 

Tachycardia vasomotoria, 345. 

Tactile sense, tests of, 385. 

Taenia echinococcus, 492. 

Taenia mediocanellata, 492. 

Taenia saginata, 492. 

Taenia solium, 491. 

Tallqvist's method of estimating 

hemoglobin, 329. 
Tape-worm, 491. 
Taste, tests for sense of, 369. 
Temperature in infectious diseases, 

21. 
Temperature, normal, 22. 
Temperature sense, tests of, 386. 
Temperature, septic type of, 68. 
Tender points of Valleix, 439. 
Tendon reflexes, 388. 
Tertian malarial fever, 47. 
Test breakfast, 242. 
Test, therapeutic, for syphilis, 441. 
Tetanella (see Tetany), 458. 
Tetanus, 80. 
Tetany, 458. 
Thermic fever, 473. 
Therapeutic test, 441. 



INDEX. 



519 



Third nerve, examination of, 366. 
Thoma-Zeiss apparatus, 325. 
Thomsen's disease, 479. 
Thoracentesis, 187. 
Thread worm, 494. 
Thrill, hydatid, 289. 
Throat, affections of, 231. 

examination of, 232. 
Thrombosis, cerebral, 402. ' 
Thrombosis, cerebral, differentiation 

from hemorrhage, 401. 
Thrombosis of portal vein, 313. 
Thrush (see Mycotic Somatitis), 233. 
Tic douloureux, 439. 
Tics, 465. 

Tics, hysterical, 447. 
Tinnitus aurium, 371. 
Tongue, examination of, 221. 
Tongue, inflammation of (see Glossi- 
tis), 233- 
Tonic spasm, 383. 
Tonsils, hypertrophy of, 235. 
Tonsillitis, 234. 

acute catarrhal, 234. 

acute follicular, 234. 

acute suppurative, 235. 

phlegmonous, 235. 
Tophi, gouty, 354. 
Torticollis, 465. 
Touch, tests of sense of, 385. 
Tracheal tug, in aortic aneurism, 

143. 
Trance, 472. 

Transverse myelitis, 421. 
Traumatic hysteria, 464. 

neurasthenia, 464. 
neuroses, 464. 
Trematodes, 493. 
Tremor, 384. 
Tremors, hysterical, 447. 
Tremor, senile, 461. 
Triceps jerk, 388. 
Trichina spiralis, 495. 
Tricocephalus dispar, 496. 



Tricuspid area, auscultation of, 117. 

insufficiency, 129. 

obstruction, 129. 

regurgitation, 129. 

stenosis, 129. 
Trigeminus nerve, 368. 
Trismus (see Tetanus), 80. 
Trismus, 369. 

Trophic phenomena of hysteria, 447. 
Tropical dysentery, 43. 
Tropho-neuroses, 466. 
Trousseau's phenomenon in tetany, 

459- 
Tubal nephritis, 211, 213. 
Tube casts in urine, 206. 
Tubercle bacillus, 87. 

methods of infec- 
tion by, 87. 
method of stain- 
ing, 101. 
formation of, 87. 
structure of, 88. 
Tubercular meningitis, 91. 
Tuberculosis, 87. 

acute, 89. 

general miliary, 89. 

general pathology of, 

87. 
miliary, 89. 
of the kidney, 221. 
of the larynx, 155. 
of the lungs, miliary, 

90. 
of the lymphatic 

glands, 92. 
pulmonary, 93. 

caseous, 94, 95. 
fibro-caseous, 

94, 97- 
fibroid, 94, 96. 
chronic, 97. 
ulcerative, 97. 

Tuberculous lymphadenitis, 92. 

Tumor, cerebral, 404. 



520 



INDEX. 



Tumor, intracranial, 404. 

of intestine, causing obstruc- 
tion, 271. 

ot the lung, 181. 
Tympanites, in typhoid, treatment 

of, 33- 
Types of fever, 20. 
Types of malarial fever, 46. 
Typhoid fever, 25. 
Typhoid state, 21. 
Typhus fever, 33. 
T}^rosin in urine, 204. 

Ulcerative pharyngitis, 237. 
Ulcer of the stomach, 253. 

tabetic, 432. 
Upper neuron, 378. 
Urates, 195, 202, 204. 
Urea, 196. 
Uremia, 208. 
Uremic asthma, 208. 
Uric acid, 197, 202. 
Uric acid diathesis (see Irregular 

Gout), 354. 
Urinary sediments, 202. 
Urinary system, diseases of, 181. 
Urine, amorphous urates in, 202. 

ammonio-magnesium phos- 
phate in, 204. 

ammonium urate in, 204. 

anatomical sediments in, 205. 

blood in, 200, 205. 

" brick dust deposit " in, 202. 

calcium oxalate in, 195, 203. 

calcium phosphate in, 204. 

casts in, 206. 

chemical examination of, 196. 

chemical sediments in, 202. 

cloudiness of, 195. 

color of, 194. 

cystin in, 203. 

epithelium in, 206. 

examination of, 193. 

incontinence of, 228. 



Urine, leucin in, 204. 

method of collecting for ex- 
amination, 193. 
microscopical examination of, 

201. 
physical examination of, 194. 
pus in, 205. 
quantity of, 194. 
reaction of, 194. 
retention of, 229. 
sedimentation of, 202. 
solids of, estimation of, 195. 
specific gravity of, 195. 
suppression of, 229. 
ty rosin in, 204. 
triple phosphate in, 204. 
uric acid in, 197, 202. 

Vaccination, 76. 
Vaccinia (see Vaccination), 77 
Valleix, tender points of, 439. 
Valvular diseases of the heart, 125. 

diagnosis of, 130. 

prognosis in, 130. 

treatment of, 131. 
Valvulitis, 123. 
Varicella, 77. 
Variola, 74. 
Varioloid, 75. 
Vasomotor phenomena of hysteria, 

447- 
Vertigo, 371. 

Vesicular emphysema, 175. 
Visceral phenomena of hysteria, 447. 
Visceroptosis, 263. 
Visual aphasia, 363, 364. 
Visual field, in hysteria, 443. 
Vision, field of, method of testing, 

365. 
Vocal cords, paralysis of, 373. 
Volvulus, 271. 
Von Fleischl's method of estimating 

hemoglobin, 329. 
Von Graefe's sign, 346. 



INDEX. 



521 



Water, conveyance of infection by, 

17- 

Water-hammer pulse, 128. 

Waxy casts in urine, 207. 

Waxy kidney, 218. 

Waxy liver, 299. 

Whip worm, 496. 

White corpuscles, forms of, 324. 

Whooping cough, 78. 

Widal test, 30. 

Wool-sorter's disease (see Anthrax), 

82. 
Word blindness, 363, 364. 



Word deafness, 363, 364. 
Worms (see Animal Parasitic Dis- 
eases), 491. 
Wrist-drop, 486. 
Wrist-jerk, 388. 
Writer's cramp, 462. 
Wry neck, 465. 

Xanthin, 197. 

Yellow atrophy of liver, 300 
Yellow fever, 41. 



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